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The size of the UK problem Stroke occurs approximately 152,000 times a year in the UK; that is one every 3 minutes 27 seconds. There are around 1.2 million stroke survivors in the UK. 3 in 10 stroke survivors will go on to have a recurrent stroke or TIA.
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► Neurological deficit (‘loss of function’) of sudden onset, lasting more than 24 hours, of vascular origin (WHO) ► Transient Ischaemic Attack less than 24 hours What is a Stroke?
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2% mass of body but 15-20% blood flow Requires O2 and glucose If starved ◦ Reduced ATP ◦ Influx of calcium ◦ Cytotoxic oedema
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Blood supply to the brain
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The carotid system supplies most of the hemispheres and cortical deep white matter The vertebro-basilar system supplies the brain stem, cerebellum and occipital lobes
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Causes of stroke ► Blockage with thrombus or clot ► Disease of vessel wall ► Disturbance of normal properties of blood ► Rupture of vessel wall (haemorrhage) ► 85% infarction ► 15% haemorrhage
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Nonmodifiable risk factors: Age Sex Ethnicity History of migraine headaches Sickle cell disease Fibromuscular dysplasia Heredity Modifiable risk factors: Hypertension (the most important) Diabetes mellitus Cardiac disease ◦ AF, valve disease, PFO, atrial and ventricular enlargement Hypercholesterolemia Transient ischemic attacks (TIAs) Carotid stenosis Hyperhomocystinaemia Lifestyle issues ◦ Excessive alcohol intake ◦ tobacco use ◦ illicit drug use ◦ Obesity ◦ physical inactivity Oral contraceptive use
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Large artery infarcts ◦ Most often the MCA ◦ Typically embolisation of athersclerotic debris Sometimes plaque ulceration and in situ thrombosis ◦ Often just proximal to major branch points Small vessel or lacunar infarction ◦ Penetrating lenticulostriate arteries Cardioembolic strokes ◦ ~20% ◦ Highest 1 month mortality
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Time of onset Witnesses Headache/ vomiting /neck stiffness/ photophobia (suggests haemorrhage) Loss of consciousness Fit Incontinence
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Stroke should be considered in any patient presenting with an acute neurologic deficit (focal or global) or altered level of consciousness. No historical feature distinguishes ischemic from hemorrhagic stroke, although nausea, vomiting, headache, and change in level of consciousness are more common in hemorrhagic strokes.
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Motor (clumsy or weak limb) Sensory (loss of feeling) Speech: Dysarthria/Dysphasia Neglect / visuospatial problems Vision: loss in one eye, or hemianopia Gaze palsy Ataxia/ vertigo / incoordination / nystagmus IN STROKE MOST SYMPTOMS ARE OF LOSS OF SOME FUNCTION
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Migraine Epilepsy Structural brain lesions ◦ SDH, Tumour, abscess Metabolic/toxic disorders ◦ hypoglycemia Vestibular disorders Psychological disorders Demyelination Mononeuropathy Bell’s Palsy
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Contralateral hemiparesis Contralateral hypaesthesia Ipsilateral hemianopia Gaze preference toward the side of the lesion. Receptive or expressive dysphasia (if dominant hemisphere) Neglect, inattention, and extinction of double simultaneous stimulation (non-dominant hemisphere) Since the MCA supplies the upper extremity motor strip, weakness of the arm and face usually worse than leg
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Primarily affects frontal lobe Disinhibition and speech perseveration, producing primitive reflexes (eg, grasping, sucking reflexes) Altered mental status Impaired judgment Contralateral weakness (greater in legs than arms) Contralateral cortical sensory deficits Gait apraxia Urinary incontinence.
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Posterior cerebral artery stroke PCA occlusions affect vision and thought ◦ contralateral homonymous hemianopsia ◦ cortical blindness ◦ visual agnosia ◦ altered mental status ◦ impaired memory. Vertebrobasilar artery occlusions are notoriously difficult to detect because they cause a wide variety of cranial nerve, cerebellar, and brainstem deficits. These include the following: ◦ Vertigo ◦ Nystagmus ◦ Diplopia ◦ Visual field deficits ◦ Dysphagia ◦ Dysarthria ◦ Facial hypaesthesia ◦ Syncope ◦ Ataxia A hallmark of posterior circulation stroke is that there are crossed findings: ipsilateral cranial nerve deficits and contralateral motor deficits. This is contrasted to anterior stroke, which produces only unilateral findings.
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Occlusion of the small, perforating arteries of the deep subcortical areas of the brain The infarcts are generally from 2-20 mm in diameter The most common lacunar syndromes include: ◦ pure motor ◦ pure sensory ◦ ataxic hemiparetic strokes By virtue of their small size and well-defined subcortical location, lacunar infarcts do not lead to impairments in cognition, memory, speech, or level of consciousness.
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Immediate management ◦ Recanalise Thrombolysis for a small number of patients if they present within 4.5 hours Intra arterial strategies ◦ Protect the penumbra Early management concentrates on: Swallowing Fluids and oxygen Early therapy involvement Good nursing care Aspirin Good evidence that organised stroke care saves lives and improves outcomes
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Ischaemic Core Ischaemic core radiates outward from the occluded area The area receiving little or no blood flow is known as the ischaemic core and is comprised of cells that die rapidly
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Ischaemic Penumbra in Acute Stroke Penumbra Infarction Functionally impaired tissue At risk of infarction Can be saved if reperfused
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Acute thrombolytic treatment aims to: - break up the occluding thrombus or embolus - restore perfusion to reversibly ischaemic brain - reduce the volume of irreversibly damaged brain tissue
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Thrombolysis in 3 hours (NINDS trial) 17.3 38.4 44.3 18.4 51.4 30.2 0 20 40 60 80 100 ThrombolysisControl Alive and independent Alive but dependent Dead Differences/1000:141 extra alive and independent(P<0.01) 130 fewer dependent survivors(P<0.01) To save 1 patient from disablement NNT is 7
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Optimising risk:benefit FAST ◦ Public ◦ High ambulance triage ◦ Prehopsital notification ROSIER ◦ High hospital triage ◦ Prompt assessment SPECIALIST STROKE ASSESSMENT
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15-item neurologic examination stroke scale Used to evaluate the effect of acute cerebral infarction on: ◦ level of consciousness ◦ extraocular movement ◦ visual-field loss ◦ motor strength ◦ ataxia ◦ sensory loss ◦ language ◦ dysarthria ◦ neglect
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CLINICAL CONTRA-INDICATIONS TO THROMBOLYSIS Previous intracranial haemorrhage, arteriovenous malformation or aneurysm History of stroke or head injury in the last 3 months Evidence of active internal bleeding History of gastrointestinal bleeding Major surgery or trauma in the last 14 days Patient has pancreatitis or pericarditis Recent lumbar puncture or arterial puncture at a non- compressible site Systolic BP > 185 mmHg; Diastolic BP > 110 mmHg
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OTHER CONTRA-INDICATIONS TO THROMBOLYSIS Haemoglobin< 10 g/dl Platelets< 100 X 10 9 /l INR> 1.4 Glucose < 2.7 Brain imaging shows: ◦ haemorrhage ◦ early infarction affecting > 1/3 MCA territory ◦ NIHSS >25
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Peri/post-thrombolysis Patient not to receive aspirin/ heparin/ warfarin for 24 hours Blood pressure to be measured: ◦ Every 15 minutes for first 2 hours ◦ Then every 30 minutes for 6 hours ◦ Then every hour for 18 hours Management of hypertension DBP>140mmHg iv sodium nitroprusside (0.5- 10mcg/kg/min) SBP>230mmHg or DBP>121-140mmHg labetalol 20mg over 2 minutes, then iv labetalol infusion (2-8mg/min) SBP 180-230 Hg or DBP 105-120mmHg labetalol 10mg over 2 minutes, then iv labetalol infusion (2-8mg/min)
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Haemorrhagic Transformation ◦ 5% of non-thrombolised ischaemic strokes Cardioembolic strokes Large infarct size Cerebral oedema Seizures Fever Neuroprotective agents? Glycaemic control?
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Up to 7% of patients having a TIA will have a further event with one month 20% of stroke survivors have another stroke within 5 years Many die of cardiovascular events
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Aspirin (+/- dipyridamole) Carotid Doppler Treat what is treatable Simvastatin 40mg, regardless of cholesterol levels ACEi and thiazide, regardless of blood pressure Aggressively investigate and treat TIAs
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ABCD2 Age >60 1 point BP >140/90 1 point Clinical features focal weakness 2 points speech 1 point Duration >60 mins 2 points 10-59 mins 1 point Diabetes 1 point
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Commence aspirin 300mg Assess ABCD2 Score >4 should have stoke assessment within 24hrs Crescendo TIAs should admit/department rv Inform DVLA- cannot drive for at least 1 month
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