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82 Cards in this Set
- Front
- Back
3rd most common cause of death
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cerebrovascular disease
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TIA
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Transient ischemic attack: a cerebrovascular event causing neurological symptoms or signs lasting less than 24 h (usually 1- 30 min).
NB: warning sign for completed stroke (5% risk in first week) |
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Types of stroke
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80% infarction
20% hemorrhage |
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Causes of Stroke
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Infarction (ischemic and hemorrhagic)
Large artery athero-thrombosis Small penetrating artery occlusion Embolism (often hemorrhagic) Global ischemia (cerebral hypoperfusion) Hemorrhage Intracerebral hemorrhage Subarachnoid hemorrhage |
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1. Large artery athero-thrombosis
SITES |
1. Extracranial vessels commonest site for atherosclerosis, especially internal carotid artery near common carotid bifurcation
2. Intracranial vessels: especially at origin of middle cerebral artery and ends of basilar artery |
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Acute Brain Infarct CHANGES
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Softening
Swelling (raised intracranial pressure can cause brain stem compression and death) Neutrophils Ischemic (“red cell”) neuronal change |
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Brain infarct: post-acute
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Foamy macrophages (start at about 3 days) - remove debris
Reactive astrocytes (start at about 10 days) - form glial scar Cavitation |
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Acute ischemia
Molecular events |
1. Decreased energy production
Failure of ionic pumps Mitochondrial injury produces free radicals 2. Glutamate release Increased intracellular calcium Stimulation of reactive intermediates leading to membrane and DNA damage |
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Brain infarct; Pathophysiology
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Neuronal electrical failure develops at 30% normal cerebral blood flow
Membrane failure develops at 15% normal cerebral blood flow Ischemic penumbra retains viability if blood flow is restored Some neurons more resistant to hypoxia (possibly due to different surface receptors) |
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2. Small penetrating artery occlusion
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aka LACUNAR INFARCT
Occlusion (arterial wall fibrous thickening or atheroma) of a small penetrating artery Causes small (up to 20 mm) infarct in deep structures of brain (basal ganglia, thalamus, internal capsule) and in the brain stem Associated with arterial hypertension Often clinically silent Over 20 clinical syndromes, especially pure sensory or motor strokes and transient ischemic attacks |
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secondary stroke or TIA prevention
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Medications
Anti-platelet agents (e.g., aspirin) Statins (many different effects) Anti-hypertensives Angioplasty or stenting |
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CADASIL
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
Presents with TIAs or migraine, can progress to subcortical dementia Notch 3 receptor gene mutations (also involved in familial hemiplegic migraine) |
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3. Embolism
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Embolic infarcts are usually peripheral in the brain
Most are hemorrhagic (due to reflow of blood into the damaged area after lysis of the thrombus). These small thrombo-emboli can by lysed (unlike large in situ thrombi) They may be multiple Most are in the middle cerebral artery territory Danger from anticoagulation therapy |
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Sources of Emboli
THROMBO-EMBOLI |
THROMBO-EMBOLI
Heart Left atrium atrial fibrillation ++ mitral stenosis Left ventricle (myocardial infarction) Valves (infective or marantic endocarditis) Artery (carotid artery, aortic arch) Venous source + cardiac septal defect Non-thrombotic emboli Atheroma, cholesterol, calcific debris (from arteries or cardiac valves) Atrial myxoma Systemic emboli (fat, air, amniotic fluid) |
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AF
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About 20% of ischemic strokes and TIAs happen in patients with atrial fibrillation
Aspirin is fairly ineffective to prevent these strokes |
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4. Global ischemia (cerebral hypoperfusion)
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“Boundary zone” infarcts seen when abrupt hypotension followed by rapid recovery
Autoregulation fails in regions most remote from the main arterial stem, between arteries territories Infarcts often seen between Middle and anterior cerebral arteries Middle and posterior cerebral arteries |
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Venous infarction/hemorrhage
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Blocked vein causes back pressure on capillaries with leakage of blood into tissue
Superior sagittal sinus especially White and grey matter affected Often seen in infants and in pregnancy Causes Local (infection, trauma) Systemic (increased coagulation, dehydration) |
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5. Intracerebral hemorrhage
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Increasing incidence in many populations (increased no. elderly, increased use of anticoagulants and anti-platelet agents)
Hematoma in cerebrum, cerebellum, or brain stem Deep intracerebral hemorrhages are associated with hypertension Hemorrhage can progress (up to 12 h) Edema around hemorrhage increases, and alters outcome Hemorrhage resolves to a “slit” lined with hemosiderin-laden macrophages |
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Intracerebral hemorrhage causes
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Arterial hypertension (deep sites)
Small artery degenerative changes ? microaneurysms Vascular malformation Capillary telangiectasia Arteriovenous malformation Hemorrhage into a brain tumour Vascular amyloid (peripheral “lobar” hemorrhage) - same amyloid as in AD (AB), ApoE genotype effect, mutation in APP causes hereditary form Systemic hemorrhagic disorder (e.g. leukemia, anticoagulants) |
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6. Subarachnoid hemorrhage
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Symptoms from
Meningeal irritation (e.g. headache) Increased intracranial pressure (e.g. decreased consciousness) Vasospasm after bleed Causes Ruptured berry aneurysm ++ Arteriovenous malformation |
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Berry Aneurysm
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Small outpouching at bifurcation of arteries
Most seen at the base of the brain (90% on anterior circulation) Thin collagenous wall Found in 2% of the population May be multiple in 25% of patients Increased incidence in first degree relatives If > 10 mm diameter, 50% risk of bleeding per year |
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Berry aneurysm
Possible pathogeneses |
1. Congenital
Medial defect at arterial bifurcation Type III collagen deficiency 2. Acquired Hemodynamic stress at bifurcation Atherosclerosis Hypertension |
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Stroke Units
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–
Acute stroke units which accept patients acutely but discharge early (usually within 7 days). – Rehabilitation stroke units which accept patients after a delay of usually 7 days or more and focus on rehabilitation; and –Comprehensive (ie combined acute and rehabilitation) stroke units - Stroke unit care includes red. neuronal cell death risk factors such as fever and hyperglycaemia |
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stroke unit outcomes
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•Reduction in death - 17%
•Reduction in death or institutionalisation - 25% •Reduction in death or dependency - 31% •Reduction in length of hospital stay - 8% •NNT to prevent death : 22 •(NNT to prevent major adverse outcome in mild hypertension : 141) •(NNT to prevent death or stroke after TIA : 6) |
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Stroke Sx
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•Amaurosis fugax (transient monocular visual loss)
•(hemi-)paresis / weakness •Sudden speaking probem • hemiapnopia • double vision |
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Stroke Mimicry
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•Seizure
•Toxic •Metabolic •Sepsis •Syncope •Confusion •Vestibular Dysfunction •Peripheral nerve lesion •Migraine |
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Stroke DDx
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•acute onset
•neurologic deficit •localizing signs •well in last week |
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TIA: last chance to prevent stroke!
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•25% risk of a vascular event or death within 90 d
•most of which occur within 48 h •10% have a major stroke within 7 days •Urgent assessment and treatment reduces the risk by 80% |
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Risk factors for stroke
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Ddx ischemic and Intracerebral hemorrhage strokes?
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Same Sx
- these people vomit a little more (unrealiable) |
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tPA Outcomes
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0 No symptoms at all
1 No significant disability despite symptoms; able to carry out all usual duties and activities 2 Slight disability; unable to carry out all previous activities, but able to look after own affairs without assistance 3 Moderate disability; requiring some help, but able to walk without assistance 4 Moderately severe disability; unable to walk without assistance and unable to attend to own bodily needs without assistance 5 Severe disability; bedridden, incontinent and requiring constant nursing care and attention 6 Dead - not increasing mortality cf to placebo even though INC> the risk of bleeds |
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Evolution of brain infarct
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Time is brain
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tPA
why 3 hrs? |
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Why do only 3% of all stroke patients receive acute treatment?
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•57% of all patients present too late (>3h) NSF Stroke audit
•Stroke doesn’t hurt •No awareness “sleep it off” |
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Endovascular Therapy
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•Ultrasound (EKOS)
•Shock-wave/ Vacuum: Angiojet •Retrieval devices (NEED, MERCI) •Laser devices (EPAR) •Suction-Devices (Penumbra) •Stent-retrievers (Solitaire) |
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Endovascular therapy after IV t-PA
VS tPA alone |
no different outcomes
- big problem is door to puncture time of greater than 2hrs |
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Aspirin + Clopidogrel?
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no comparitive benefit
+ added risk esp, if the stroke is haemorrhagic |
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RR of Stroke in AF
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Warfarin vs Placebo 62% (48 - 72%) ASA vs Placebo 22% (2 - 38%) Warfarin vs ASA 36% (14 - 52%) |
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Aggressive medical managment of IC stenosis vs Stenting
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STENTING; doubles risk of stroke initially but then no added risk thereafter WHEREAS
medical therapy groups slowly catch up in the longer term |
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What predicts survival/recovery?
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•Age
•Gender •Severity of illness / condition - HT is greatest risk factor •Pre-existing illness or disability •Use of effective treatments •Compliance with effective treatments •Issues related to general health smoking alcohol physical activity nutritional status adequate income marital status |
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Rule of 1/3
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1 year after stroke
•1/3 die •1/3 recover •1/3 have persistent disability |
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Prognosis after a stroke
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lots of people die early on then they seem to be parallel
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what time of day do stroke mostly occur?
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mornings
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risk if having a stroke following a TIA
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1 in 5
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ABCD2
score |
• Age 60 years or older (1point)
• Blood pressure elevation on first assessment after TIA -systolic ≥140 mmHg or diastolic ≥90 mmHg (1point) • Clinical features of TIA (unilateral weakness, 2points; or speech impairment without weakness, (1point) • Duration of TIA ≥60 minutes, 2 points; or 10–59 minutes (1 point) • Diabetes (1 point) |
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Assessing TIA or stroke
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1. ischaemic or hemorrhage
2. vascular territory involved 3. Pathophysiology of the event 4. vascular risk factors 5. Assoc. vascular disease |
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Stroke Ix
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1. brain imaging (CT or MRI)
2. vascular imaging- carotid/vertebrobasilar US or CT/MRI angiogram 3. ECG, Echo 4. Blood test - coag screen, cholestrol... |
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Treating an assymptomatic carotid stensois
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- 1% risk reduction per year
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Secondary prevention following minor stroke or TIA due to carotid stenosis
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emergency surgery therefore required
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Carotid endarterectomy
or carotid stent? |
- similar rates of death within 30days of surgery, there is a trend though towards surgerybeing more effective
- and after 2yrs similar rates of recurrent ipisilaterals |
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Antiplatelet MOA
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Aspirinr RR
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13% for stroke
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Clopidigrel vs Aspirin
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RRR; 7.3%
- fewer ICH and haemorrhagic deaths too |
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When do you use clopidogrel?
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- more expensive thus use only when
- risk of GI complications - an event has occured while on aspirin |
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Dipyridamole and
Aspirin in secondary prevention of stroke |
RR compared to placebo
DP; 16% ASA: 18% DP + ASA: 37% - when together doubles RR and no added SE, no added haemorragic SE, except the headache at Tx initation - also still cheaper than clopidogrel |
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ASA + Clopidogrel
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- the combo was not significantly more effective than aspirin alone in reducing rates of MI, stroke, or death (CV)
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Warfarin vs ASA
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-no benefit over ASA in patients without AF or other cardiac sources of emboli
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AF risk stratification
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Dabigatran vs Warfarin
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lower embolism or stroke: 1.11%/year vs 1.69%
- lower rates of haemorragic stroke (0.12% vs 0.38%) problem; \no inhibitor of dabigatran / no test for anti-coag activity |
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Are all anti-hypertensives equally effective for secondary stroke prevention?
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- diuretiics, b-blockers, CCB, ACEI, AT2A
all effective |
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What BP should be targeted?
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130/85 is hypertensive (ASA)
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Statsins
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effective in reducing
- major coronary - any stroke (may be an inc. in haemorrhagic stroke) - revascularisation by 1/3 irrespective of age, sex, cholestrol level, other Tx |
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Cholestrol Targets
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<4 total
<2.5 LDL |
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Smoking
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INC risk
- 3.7 x stroke - 9,8 x subarachnoid haemorrhage STOP smoking the risk drops to baseline by 3-5yrs |
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EtOH
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- heavy use INC. stroke
- haemorrhage assoc. with binge - moderate use protective (INC. HDL) 1-1.2 STD female and 2 for males |
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OC & HRT
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RR: 2.75 in OC (lower the dose of E lower the risk)
RR: 1.2 in HRT but mortality unaffected |
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Cortical Sx of stroke
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anosagnosie
sensory neglect dysarthria... |
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Why is stroke a medical emergency?
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- ischaemic penumbra
- not yet reached the point energy and ion pump failure where the tissue can no longer maintain integrity |
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DW-MRI
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- maps avergae apparent diffusion coefficient (ADC)
- ADC is red. following a stroke due to cytotoxic oedema (can tell within minutes), normal at week 1 and after that ADC increases - can be combine with PWI using gadolinium to ID brain tissue that is reduced perfusion but not infarcted (Ischaemic Pneumbra) |
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rTPA
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- 30% more likely to have minimal or no disability at 3 months
- mortality 17% and 21% placebo - symptomatic ICH within 36hrs 6.4% rTPA vs 0.6% placebo - significant benefit upto 4.5hrs |
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MERCI Clot retriever
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Maintenance of perfusion- HT following stroke
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- autoregulation of cerebral perfusion is lost with acute stroke
- thus DONT lower BP after a stroke until it reaches levels that will cause organ damage |
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Insulin, BG and stroke
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- hyperglycemia in acute phase related to poor outcome
- insulin has direct protective effect on cerebral ischaemia (IGF-1 mediated) |
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Fever + Stroke
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elevated temp in acute pahse ahs worse outcomes
- lower temp with paracetamol + cooling |
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Anticoagulation following cardioembolic stroke due to AF
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- when to start
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Stroke unit NNT
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32 for survival
18 to regain independence 16 to return home |
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Essential early care in stroke
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- document deficits and evalute risk
- estab. pathophysiology and Mx, Px - Est. Swallowing and prevent aspiration - monitor vitals - adquate nutrition and fluids - establish communication - bladder and bowels (avoiding catheterization) - BP managment - harm minimization - min. distress (emotional) - approp. info |
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Relative Efficacy of Stroke Tx
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NNT
tPA <3hrs = 7 tPA <6hrs = 11 stroke unit = 18 aspirin = 83 |
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Cogn. Deficit
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- usually improve after stroke
- recogn. and appropriate Mx of depression as a major impediment to rehab |
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Rehab
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MAX. acheived after 12wks (no more improvement should be expected after 5 months)
begin ASAP |
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Salt
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AVg. red. in BP by 5-7mmHg in HT below 90mmol/day
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