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2444755436870Aetiology00Aetiology1550670752348025%Haem-orrhage0025%Haem-orrhage2399665752348050% intracerebral (???2x more common than SAH)50% SAH30-50% deathPrimary (80-90%) Spontaneous rupture of small blood vessel by chronic HTN or amyloid angiopathy) Putamen > thalamus > pons > cerebellum, upper brainstem, basal ganglia (HTN Charcout-Bouchard microaneurysms of penetrating arteries of MCA, basal and COW) haemorrhage that evolves over few mins which is central location on CT Secondary (10-20%) 50% due to AVM, aneurysms, bleeding diathesis, lesion (eg. cancer), extension of SAH 50% idiopathic lobar haemorrhage which have rapid onset symptoms with focal headache which is more likely to be peripheral location on CT0050% intracerebral (???2x more common than SAH)50% SAH30-50% deathPrimary (80-90%) Spontaneous rupture of small blood vessel by chronic HTN or amyloid angiopathy) Putamen > thalamus > pons > cerebellum, upper brainstem, basal ganglia (HTN Charcout-Bouchard microaneurysms of penetrating arteries of MCA, basal and COW) haemorrhage that evolves over few mins which is central location on CT Secondary (10-20%) 50% due to AVM, aneurysms, bleeding diathesis, lesion (eg. cancer), extension of SAH 50% idiopathic lobar haemorrhage which have rapid onset symptoms with focal headache which is more likely to be peripheral location on CT1551940592264575%Infarction0075%Infarction2399665592264550% unknown25% lacunar (due to lipohyalinosis, associated with diabetes and HTN)20% embolic (eg. Mural / valve disease; embolisation more common than in TIA; more commonly present on activity)5% atherosclerotic (more commonly present on awakening)Also gas embolism, dissection (10-25% CVA’s in young/middle aged); hypotension / perfusion (causes CVA in watershed area)60% infarcts become haemorrhagic10% death0050% unknown25% lacunar (due to lipohyalinosis, associated with diabetes and HTN)20% embolic (eg. Mural / valve disease; embolisation more common than in TIA; more commonly present on activity)5% atherosclerotic (more commonly present on awakening)Also gas embolism, dissection (10-25% CVA’s in young/middle aged); hypotension / perfusion (causes CVA in watershed area)60% infarcts become haemorrhagic10% death15506705442585Thromboembolism is most common at bifurcation of ICA; atherosclerosis most common at origin of ICATIA: inflammatory; hyperviscosity; subclavian steal; sympathomimetics; and causes below…00Thromboembolism is most common at bifurcation of ICA; atherosclerosis most common at origin of ICATIA: inflammatory; hyperviscosity; subclavian steal; sympathomimetics; and causes below…155067045758101Y prevention: HTN most important; also DM, smoking, ? chol, AF, endocarditis, multiple sclerosis, prosthetic heart valves, male, ? age, heart diseaseICH: HTN (DBP >95), XS ETOH, aneurysm, anticoagulation, cocaine, intracranial SOL, amyloid angiopathySickle cell canaemia most common cause of CVA in children001Y prevention: HTN most important; also DM, smoking, ? chol, AF, endocarditis, multiple sclerosis, prosthetic heart valves, male, ? age, heart diseaseICH: HTN (DBP >95), XS ETOH, aneurysm, anticoagulation, cocaine, intracranial SOL, amyloid angiopathySickle cell canaemia most common cause of CVA in children2444754575810Risk Factors00Risk Factors2451103107055Patho-physiology00Patho-physiology15513053107055Brain receives 15% CO, 25% O2 consumption, 70% glucose<20ml/min/100g reversible ischaemia, absent EEG activity<10-15ml/min/100g cell death, stop ATP synthesis, ion pump stopsIschaemic penumbra: threatened but potentially salvageable brain surrounding infarct00Brain receives 15% CO, 25% O2 consumption, 70% glucose<20ml/min/100g reversible ischaemia, absent EEG activity<10-15ml/min/100g cell death, stop ATP synthesis, ion pump stopsIschaemic penumbra: threatened but potentially salvageable brain surrounding infarct161290031642052451102246630Definition00Definition15513052246630TIA: FND lasting <24hrs or “a brief episode of neurological dysfunction caused by focal brain/retinal ischaemia with clinical symptoms usually lasting <1hr, without evidence of acute infarction”Cerebral infarct: thrombotic / embolic occlusion of major intracranial blood vessel; acute non-reversing loss of brain function due to vascular event00TIA: FND lasting <24hrs or “a brief episode of neurological dysfunction caused by focal brain/retinal ischaemia with clinical symptoms usually lasting <1hr, without evidence of acute infarction”Cerebral infarct: thrombotic / embolic occlusion of major intracranial blood vessel; acute non-reversing loss of brain function due to vascular event245110965200Epidemiology00Epidemiology1551305964565TIA: early investigation and intervention can prevent 80% early CVA’sCVA: 3rd highest cause of death in developed countries; incidence doubles every decade over 55yrs; variable outcome; 20% need institutional care for >3/12; 20% remain permanently disabled; death 10%; 55% discharge homeICH: death 30-50% (50% deaths within 48hrs; >80% if on warfarin); 33% discharge home; 30% 1yr survival; ICH more common in menLacunar: death low; 30% long term disability00TIA: early investigation and intervention can prevent 80% early CVA’sCVA: 3rd highest cause of death in developed countries; incidence doubles every decade over 55yrs; variable outcome; 20% need institutional care for >3/12; 20% remain permanently disabled; death 10%; 55% discharge homeICH: death 30-50% (50% deaths within 48hrs; >80% if on warfarin); 33% discharge home; 30% 1yr survival; ICH more common in menLacunar: death low; 30% long term disability246380330200CVA00CVA294640511175Assessment00Assessment1590040511175Ischaemic CVA00Ischaemic CVA24390356243955Post-eriorCirc-ulation00Post-eriorCirc-ulation31648407947025Vertebrobasilar00Vertebrobasilar36988757946390Region: cerebellum, brainstemSymptoms: ataxia, dizziness, nausea and vomiting, vertigo Nystagmus, diplopia, internuclear opthalmoplegia Facial weakness Dysarthria Ipsilateral CN signs, contralateral body signsLateral medullary syndrome (Wallenberg’s): ipsilateral UMN Horner’s syndrome, loss of pain and temperature sensation to face including loss of corneal reflex); contralateral loss of pain and temperature in body; dysphagia, dysarthria, dysphonia (IX, X); conjugate gaze palsy, vertigo, nystagmus, ataxiaLocked in syndrome: basilar artery00Region: cerebellum, brainstemSymptoms: ataxia, dizziness, nausea and vomiting, vertigo Nystagmus, diplopia, internuclear opthalmoplegia Facial weakness Dysarthria Ipsilateral CN signs, contralateral body signsLateral medullary syndrome (Wallenberg’s): ipsilateral UMN Horner’s syndrome, loss of pain and temperature sensation to face including loss of corneal reflex); contralateral loss of pain and temperature in body; dysphagia, dysarthria, dysphonia (IX, X); conjugate gaze palsy, vertigo, nystagmus, ataxiaLocked in syndrome: basilar artery243903551117530% LOC (major altered LOC suggests bilaterally hemispheric / brainstem dysfunction)0030% LOC (major altered LOC suggests bilaterally hemispheric / brainstem dysfunction)316420591694080% brain; ICA + ACA + MCA + ophthalmic; 80% CVA’s are MCA territory; supplies frontal lobe, parietal lobe, most of temporal lobe (anterior and medial cortex), optic nerve significant oedema, decreased LOC0080% brain; ICA + ACA + MCA + ophthalmic; 80% CVA’s are MCA territory; supplies frontal lobe, parietal lobe, most of temporal lobe (anterior and medial cortex), optic nerve significant oedema, decreased LOC36982401700530Region: parietal, some temporal, Broca’s (speaking), Wernicke’s (understanding)Aetiology: embolicSymptoms: contralateral hemiplegia / sensory loss face (UMN pattern) + arm > leg Eyes deviated towards Contralateral homonymous hemianopia L (dominant) expressive (anterior) or receptive (posterior) aphasia, agnosia, agraphia, acalculia, L-R disorientation R (non-dominant) L sided neglect, spatial neglect, dressing apraxia00Region: parietal, some temporal, Broca’s (speaking), Wernicke’s (understanding)Aetiology: embolicSymptoms: contralateral hemiplegia / sensory loss face (UMN pattern) + arm > leg Eyes deviated towards Contralateral homonymous hemianopia L (dominant) expressive (anterior) or receptive (posterior) aphasia, agnosia, agraphia, acalculia, L-R disorientation R (non-dominant) L sided neglect, spatial neglect, dressing apraxia31642051700530MCA80%00MCA80%36976053568065Region: medial frontal and parietal, basal ganglia, internal capsule, olfactory bulbEpidemiology: rare as good collateral from anterior communicating arterySymptoms: contralateral hemiplegia (but NO sensory loss) Leg > arm Difficulty initiating movement Confusion, personality changes Abnormal conjugate gaze Grasp / pout / palmomental reflex; urinary incontinence; gait; smell; sensory / visual inattention L (dominant) speech problems (difficulty initiating) R (non-dominant) confusion, neglect00Region: medial frontal and parietal, basal ganglia, internal capsule, olfactory bulbEpidemiology: rare as good collateral from anterior communicating arterySymptoms: contralateral hemiplegia (but NO sensory loss) Leg > arm Difficulty initiating movement Confusion, personality changes Abnormal conjugate gaze Grasp / pout / palmomental reflex; urinary incontinence; gait; smell; sensory / visual inattention L (dominant) speech problems (difficulty initiating) R (non-dominant) confusion, neglect31635703568065ACA00ACA31642055764530Opthalmic00Opthalmic36976055764530Symptoms: monocular visual loss (amourosis fugax)00Symptoms: monocular visual loss (amourosis fugax)2438400920115AnteriorCirc-ulation00AnteriorCirc-ulation3164840624078020% brain; vertebral + basilar + PCASupplies cerebellum, brainstem, thalamus, occipital lobe, some of temporal lobe (medial), auditory and vestibular0020% brain; vertebral + basilar + PCASupplies cerebellum, brainstem, thalamus, occipital lobe, some of temporal lobe (medial), auditory and vestibular36988756858635Region: occipital lobe, some temporalSymptoms: hemisensory loss (but NO motor weakness) Homonymous hemianopia, quadrantanopia, cortical blindness (if bilateral) Dyslexia, memory loss Ipsilateral III palsy00Region: occipital lobe, some temporalSymptoms: hemisensory loss (but NO motor weakness) Homonymous hemianopia, quadrantanopia, cortical blindness (if bilateral) Dyslexia, memory loss Ipsilateral III palsy31648406858635PCA00PCA369697012068810Symptoms: monocular visual loss (amourosis fugax)00Symptoms: monocular visual loss (amourosis fugax)316357012068810Opthalmic00Opthalmic2946405962650Assessing TIA Risk:ABCD2 Score00Assessing TIA Risk:ABCD2 Score1600835596265020-25% will have CVA in next year; 30% with TIA will have CVA within 5 years (5% in 48hrs, 10% in 1/12, 10-20% in 90/7)ABCD score: 2-5% 1/52 risk if <5; 35-55% if 6California score: age, diabetes, duration, weakness, speech impairmentAdmit TIA if: ABCD2 score >4; 4 TIA’s in 2/52; 3 TIA’s in 72hrs; 2 TIA’s in 24hrs; high grade carotid stenosis; ?cardiac source; embolic TIA despite anticoagulation0020-25% will have CVA in next year; 30% with TIA will have CVA within 5 years (5% in 48hrs, 10% in 1/12, 10-20% in 90/7)ABCD score: 2-5% 1/52 risk if <5; 35-55% if 6California score: age, diabetes, duration, weakness, speech impairmentAdmit TIA if: ABCD2 score >4; 4 TIA’s in 2/52; 3 TIA’s in 72hrs; 2 TIA’s in 24hrs; high grade carotid stenosis; ?cardiac source; embolic TIA despite anticoagulation57207157115810<4 do CT head and carotid USS within 48-72 hours; outpatient follow up>4 admit; do CT / MRI within 24 hoursRisk of stroke0-3 = low risk = 1% 2/7, up to 15% 1/524-5 = mod risk = 4% 2/7, 20-25% 1/526-7 = high risk = 8% 2/7, 25-30% 1/5200<4 do CT head and carotid USS within 48-72 hours; outpatient follow up>4 admit; do CT / MRI within 24 hoursRisk of stroke0-3 = low risk = 1% 2/7, up to 15% 1/524-5 = mod risk = 4% 2/7, 20-25% 1/526-7 = high risk = 8% 2/7, 25-30% 1/5221101057115810Age >60 years00Age >60 years21082007439660BP >140/9000BP >140/9021075659230360Diabetes00Diabetes422084592303601 point001 point421894085826601 point001 point422084589268302 points002 points421894082188052 points002 points421894077724001 point001 point28136858218805Unilateral weakness00Unilateral weakness28136857764145Speech impairment without weakness00Speech impairment without weakness420687571164451 point001 point420878074402951 point001 point16008359230995D00D16008358582660D00D21031208579485Duration00Duration28136858929370> 60 minutes00> 60 minutes2814320858266010 – 60 minutes0010 – 60 minutes16008357767320C00C21031207764145Clinical features00Clinical features16046457439660B00B16027407116445A00A2946405287010Differential Diagnosis00Differential Diagnosis16008355286375Seizures (20%; especially in elderly or previous CVA), sepsis (13%), toxic/metabolic (eg. hypoglycaemia, drugs, hypoxia, hyponatraemia; 11%); SOL (9%); syncope (9%)Others: migraine, cancer, SDH, herpes encephalitis, neuropathy, psychogenic, aortic dissection00Seizures (20%; especially in elderly or previous CVA), sepsis (13%), toxic/metabolic (eg. hypoglycaemia, drugs, hypoxia, hyponatraemia; 11%); SOL (9%); syncope (9%)Others: migraine, cancer, SDH, herpes encephalitis, neuropathy, psychogenic, aortic dissection294640477520Assessment00Assessment24371304292600Symptoms: usually last 2-15mins, rarely >1hr; sudden onset without warning, max in minutesExamination: usually normal; look for evidence of cardiac / vascular disease; carotid bruit 75% sensitive and >75% specific for mod-high grade stenosis; 90% carotid bruits are mod-high degree, 5-10% are surgically amenable; high risk lesion if diastolic component00Symptoms: usually last 2-15mins, rarely >1hr; sudden onset without warning, max in minutesExamination: usually normal; look for evidence of cardiac / vascular disease; carotid bruit 75% sensitive and >75% specific for mod-high grade stenosis; 90% carotid bruits are mod-high degree, 5-10% are surgically amenable; high risk lesion if diastolic component15881354292600TIA00TIA15881351928495Haem-orrhagic CVA00Haem-orrhagic CVA24371301927859Tends to have more nausea, vomiting, headache; tends to have slow onset; LOC often impaired; 25% are initially alert then deteriorate over 24 hours; high mortality if blood in ventriclesPutamen: contralateral hemiplegia with no sensory loss eyes deviate to contralateral sideThalamic: contralateral hemiplegia and sensory loss Eye down and in; unequal pupils; absent light reflex; ipsilateral Horner’s syndrome; lateral gaze defect AphasiaPons: quadriplegia; decerebrate rigidity (decorticate in medulla / midbrain) Pinpoint pupils Deep coma, tachypnea, HTN, hyperhidrosisCerebellar: eyes deviate to contralateral side Vomiting, vertigo00Tends to have more nausea, vomiting, headache; tends to have slow onset; LOC often impaired; 25% are initially alert then deteriorate over 24 hours; high mortality if blood in ventriclesPutamen: contralateral hemiplegia with no sensory loss eyes deviate to contralateral sideThalamic: contralateral hemiplegia and sensory loss Eye down and in; unequal pupils; absent light reflex; ipsilateral Horner’s syndrome; lateral gaze defect AphasiaPons: quadriplegia; decerebrate rigidity (decorticate in medulla / midbrain) Pinpoint pupils Deep coma, tachypnea, HTN, hyperhidrosisCerebellar: eyes deviate to contralateral side Vomiting, vertigo1588135481965Ischaemic CVA(cntd)00Ischaemic CVA(cntd)2437130485140Lacunar00Lacunar3151505481330Region: basal ganglia, pons, cerebellum, anterior internal capsule, deep cerebral white matterSymptoms: localized sensory / motor defects (eg. Pure sensory, pure motor, clumsy hand) Internal capsule contralateral motor loss, no sensory loss Thalamus / pons sensory loss, no motor weakness Pons hand clumsiness and dysarthriaManagement: aspirin less helpful; good prognosis00Region: basal ganglia, pons, cerebellum, anterior internal capsule, deep cerebral white matterSymptoms: localized sensory / motor defects (eg. Pure sensory, pure motor, clumsy hand) Internal capsule contralateral motor loss, no sensory loss Thalamus / pons sensory loss, no motor weakness Pons hand clumsiness and dysarthriaManagement: aspirin less helpful; good prognosis2946402581275Investigation00Investigation16008352580640Bloods: electrolytes, BSL, FBC; ABG’s if respiratory depression; ESR if vasculitis suspected or age <40yrsECG: arrhythmia, MI; AF most common in TIACXR: exclude aortic dissection, aspiration, intrathoracic cancerCT head: In TIA: low yield In CVA: if infarct, no abnormality in 1st few hours (sensitivity 50% at 6hrs, specificity >95%) Early changes suggest large infarct: loss of grey-white differentiation is 1st sign, parenchymal hypodensity, effacement of sulci, ventricular compression, local mass effect, loss of insular ribbon, obscuration of lentiform nucleus, hyperdense MCA or other (100% specificity, 30% sensitivity for MCA) hypoattenuation at 24 hours (max at 3-5/7) increased attentuation (for few weeks) decreased attenuation with mass effect and ill defined margins isodense at 1-2/52 more decreased attenuation looks like CSF at few months Poor outcome with thrombolysis if: hypodensity >1/3 MCA territory (19% fatal haemorrhage vs 0%; 7% good 3/12 outcome vs 17%), sulcal effacement, mass effect, cerebral oedemaIn ICH: increased attenuation in 1st week (hypodense area may be active bleeding) decreased density and blurring of margins from periphery after 1/52 surrounding oedema (may contrast enhance mimicking cancer) loss of mass effect isodense at 3/52 hypoattentuation at 10/52 little residual change Repeat in 24hrs will show increase in haematoma size in 30% (associated with poor prognosis)ASPECTS: CT score for use in MCA CVA; score <7 predicts worse functional outcome at 3/12 and symptomatic haemorrhage Hypodense Hyperdense Isodense Hypodense .CVA Maybe very early For few wks 1-2/52 Few months Contrast enhances from 4/7 – 8/52ICH Active bleeding 1st wk 3/52 10/52 SDH Active bleeding Initial 1-3/52 4-6/52 .Perfusion CT: may detect lesions that will have poor results with thrombolysis, allowed measurement of cerebral blood flow as predictor of stroke progression or resolution, can show cerebral ischaemia within 1-2 hours, only takes a few minutes, will show potentially reversible penumbra, may need double contrast bolus dose; especially do if peripheral ICH to determine source of haemorrhageMRA: 80% sensitivity, 95% specificity for carotid stenosis >50%; may detect lesions that will have poor results with thrombolysis, allowed measurement of cerebral blood flow as predictor of stroke progression or resolutionMRI: more sensitive (especially in posterior territory / brainstem CVA; and for ICH >1/52 from onset), but may delay treatment; less widely availableDiffusion MRI: can detect ischaemia within 2hrs; 75% sensitivity in 3hrs, >95% sensitivity >3hrs, >95% specificityPerfusion MRI: diffusion-perfusion mismatch idenitifies salvageable penumbra and can more accurately i idenitify those likely to benefit from thrombolysisTranscranial Doppler USS: rapid, but need expertise; can assess MCACarotid Doppler USS: do if suspected ant circulation TIA; 85% sensitive, 90% specific for >70% stenosisEcho: if evidence of structural cardiac disease OE/ECG/CXR, or suspect emboli (eg. AF, recent MI); low yield otherwiseHolter: if no other cause for TIA found00Bloods: electrolytes, BSL, FBC; ABG’s if respiratory depression; ESR if vasculitis suspected or age <40yrsECG: arrhythmia, MI; AF most common in TIACXR: exclude aortic dissection, aspiration, intrathoracic cancerCT head: In TIA: low yield In CVA: if infarct, no abnormality in 1st few hours (sensitivity 50% at 6hrs, specificity >95%) Early changes suggest large infarct: loss of grey-white differentiation is 1st sign, parenchymal hypodensity, effacement of sulci, ventricular compression, local mass effect, loss of insular ribbon, obscuration of lentiform nucleus, hyperdense MCA or other (100% specificity, 30% sensitivity for MCA) hypoattenuation at 24 hours (max at 3-5/7) increased attentuation (for few weeks) decreased attenuation with mass effect and ill defined margins isodense at 1-2/52 more decreased attenuation looks like CSF at few months Poor outcome with thrombolysis if: hypodensity >1/3 MCA territory (19% fatal haemorrhage vs 0%; 7% good 3/12 outcome vs 17%), sulcal effacement, mass effect, cerebral oedemaIn ICH: increased attenuation in 1st week (hypodense area may be active bleeding) decreased density and blurring of margins from periphery after 1/52 surrounding oedema (may contrast enhance mimicking cancer) loss of mass effect isodense at 3/52 hypoattentuation at 10/52 little residual change Repeat in 24hrs will show increase in haematoma size in 30% (associated with poor prognosis)ASPECTS: CT score for use in MCA CVA; score <7 predicts worse functional outcome at 3/12 and symptomatic haemorrhage Hypodense Hyperdense Isodense Hypodense .CVA Maybe very early For few wks 1-2/52 Few months Contrast enhances from 4/7 – 8/52ICH Active bleeding 1st wk 3/52 10/52 SDH Active bleeding Initial 1-3/52 4-6/52 .Perfusion CT: may detect lesions that will have poor results with thrombolysis, allowed measurement of cerebral blood flow as predictor of stroke progression or resolution, can show cerebral ischaemia within 1-2 hours, only takes a few minutes, will show potentially reversible penumbra, may need double contrast bolus dose; especially do if peripheral ICH to determine source of haemorrhageMRA: 80% sensitivity, 95% specificity for carotid stenosis >50%; may detect lesions that will have poor results with thrombolysis, allowed measurement of cerebral blood flow as predictor of stroke progression or resolutionMRI: more sensitive (especially in posterior territory / brainstem CVA; and for ICH >1/52 from onset), but may delay treatment; less widely availableDiffusion MRI: can detect ischaemia within 2hrs; 75% sensitivity in 3hrs, >95% sensitivity >3hrs, >95% specificityPerfusion MRI: diffusion-perfusion mismatch idenitifies salvageable penumbra and can more accurately i idenitify those likely to benefit from thrombolysisTranscranial Doppler USS: rapid, but need expertise; can assess MCACarotid Doppler USS: do if suspected ant circulation TIA; 85% sensitive, 90% specific for >70% stenosisEcho: if evidence of structural cardiac disease OE/ECG/CXR, or suspect emboli (eg. AF, recent MI); low yield otherwiseHolter: if no other cause for TIA found1602740273685ROSIER scale: GCS, BP, BSL, LOC/syncope, seizure, facial / arm / leg weakness, speech, visual field defectPros: validated specifically for ED after triage; recommended by NICS, NSF, NICE, SIGN; if score <0, sensitivity 90-95%, specificity 75-90% for stroke unlikelyFAST: facial movement, arm movement, speech, testPros: used pre-hospital to allow patients to be taken to stroke centresOthers: CPSS, LAPSS, MASS00ROSIER scale: GCS, BP, BSL, LOC/syncope, seizure, facial / arm / leg weakness, speech, visual field defectPros: validated specifically for ED after triage; recommended by NICS, NSF, NICE, SIGN; if score <0, sensitivity 90-95%, specificity 75-90% for stroke unlikelyFAST: facial movement, arm movement, speech, testPros: used pre-hospital to allow patients to be taken to stroke centresOthers: CPSS, LAPSS, MASS296545274320Stroke Screening Tools00Stroke Screening Tools16008351751330NIH stroke scale: Pros: quick, reproducible, correlates with infarct volume, measures level of impairment; allows comparison of deficit over timeCons: weighted towards anterior circulation00NIH stroke scale: Pros: quick, reproducible, correlates with infarct volume, measures level of impairment; allows comparison of deficit over timeCons: weighted towards anterior circulation2946401751965Stroke Assessment Tools00Stroke Assessment Tools2946401060450Management00Management16008353591560Ischaemic CVA00Ischaemic CVA24638003591560BP: aggressive BP lowering may decrease cerebral perfusion and worsen stroke Lower BP if consistently >220 / >120-140 or MAP >130 (if for thrombolysis, need BP <185/110 to meet criteria) aim 10-15% decrease in BP within 24 hoursAntiplatelet: commence aspirin (clopidogrel if contraindicated; delay 24 hours if thrombolysed); decreased risk of early death and recurrent CVA (Chinese acute stroke trial); beneficial as secondary prevention; no evidence for heparin; warfarin later if AFThrombolysis: to salvage penumbra if commenced within <3 hours Dose: 0.9mg/kg tPA (max 90mg), 10% as bolus, 90% over 60 minutes admit stroke unit / HDU bed check BP Q15min for 2 hours Q30mins for 6 hours Q1hr for 16 hours Contraindications: unknown time of onset; improving symptoms; minor (NIHSS <4); major (NIHSS >25); SBP >185; DBP ?110; high risk CT findings (>1/3 MCA territory, multilobar infarction); seizure; platelets <100; PT >15; BSL <2.7 / >22.2; symptoms suggestive of SAH; heparin in last 48 hours; increased APTT; unable to consent; >3 hours; >80 years age; demonstrable perfusion Pros: benefits at 3-12/12; NNT 8; if used <90mins, NNT 4.5; if 90-180mins, may be minimal functional benefit; if 3 – 4.5hrs, marginal; independent reviewers support use; small number of eligible patients so minimal disruption to ED function Cons: early mortality risk; insufficient evidence to draw conclusions about effect of thrombolysis in unselected patient; only 2 trials showed positive effect and they have poorly matched groups favouring tPA; industry sponsored trials with small cohorts; all other trials have showed no benefit of harm (ASK, MAST-I, MAST-E (all used SKA) all ceased early due to increased mortality risk); no data if >80rs; small number of patients studied in few trials (more in MI); patients rarely fit criteria (eg. Time to presentation; 5% eligible, with potential for benefit in 2.3%, so benefit in 0.4% all patients presenting to hospital); less helpful in lacunar / large vessel CVA’s; no improvement in 1st 24 hours; 75% patients will improve with placebo; unlikely benefit in lacunar syndromes / large vessel occlusion; if used 90-180mins, may increase mortality 1%, if 3-4.5hrs, 1% absolute increased mortality; may disrupt care of other patients (including from post-thrombolysis cares); stroke mimics (where thrombolysis can only be bad) valid consent difficult to obtain; maybe less cost effective than other strategies; potential for protocol violation (eg. Treat after 3hrs); difficult work up (easy in MI); short time frame (6hrs in MI); unknown magnitude of treatment effect, duration of therapeutic window, which patients will benefit00BP: aggressive BP lowering may decrease cerebral perfusion and worsen stroke Lower BP if consistently >220 / >120-140 or MAP >130 (if for thrombolysis, need BP <185/110 to meet criteria) aim 10-15% decrease in BP within 24 hoursAntiplatelet: commence aspirin (clopidogrel if contraindicated; delay 24 hours if thrombolysed); decreased risk of early death and recurrent CVA (Chinese acute stroke trial); beneficial as secondary prevention; no evidence for heparin; warfarin later if AFThrombolysis: to salvage penumbra if commenced within <3 hours Dose: 0.9mg/kg tPA (max 90mg), 10% as bolus, 90% over 60 minutes admit stroke unit / HDU bed check BP Q15min for 2 hours Q30mins for 6 hours Q1hr for 16 hours Contraindications: unknown time of onset; improving symptoms; minor (NIHSS <4); major (NIHSS >25); SBP >185; DBP ?110; high risk CT findings (>1/3 MCA territory, multilobar infarction); seizure; platelets <100; PT >15; BSL <2.7 / >22.2; symptoms suggestive of SAH; heparin in last 48 hours; increased APTT; unable to consent; >3 hours; >80 years age; demonstrable perfusion Pros: benefits at 3-12/12; NNT 8; if used <90mins, NNT 4.5; if 90-180mins, may be minimal functional benefit; if 3 – 4.5hrs, marginal; independent reviewers support use; small number of eligible patients so minimal disruption to ED function Cons: early mortality risk; insufficient evidence to draw conclusions about effect of thrombolysis in unselected patient; only 2 trials showed positive effect and they have poorly matched groups favouring tPA; industry sponsored trials with small cohorts; all other trials have showed no benefit of harm (ASK, MAST-I, MAST-E (all used SKA) all ceased early due to increased mortality risk); no data if >80rs; small number of patients studied in few trials (more in MI); patients rarely fit criteria (eg. Time to presentation; 5% eligible, with potential for benefit in 2.3%, so benefit in 0.4% all patients presenting to hospital); less helpful in lacunar / large vessel CVA’s; no improvement in 1st 24 hours; 75% patients will improve with placebo; unlikely benefit in lacunar syndromes / large vessel occlusion; if used 90-180mins, may increase mortality 1%, if 3-4.5hrs, 1% absolute increased mortality; may disrupt care of other patients (including from post-thrombolysis cares); stroke mimics (where thrombolysis can only be bad) valid consent difficult to obtain; maybe less cost effective than other strategies; potential for protocol violation (eg. Treat after 3hrs); difficult work up (easy in MI); short time frame (6hrs in MI); unknown magnitude of treatment effect, duration of therapeutic window, which patients will benefit16008351059815ED stroke and TIA care bundle: rapid initial stroke screen; ABCD2 if TIA; urgent CT/MRI; NBM until swallow assessed; aspirin as soon as ICH excluded; monitor neurological status, BSL, BP, hydration statusStroke units: single most important recommendation in stroke by National Stroke Foundation; significantly decrease death and disability, more adherance to key principles, more patients eligible for stroke unit than thrombolysis so more impact; interdisciplinary team, early mobilisation, avoid bed rest, active encouragementA: may not be suitable for ETT; elevate head of bed 30 degreesB: no clear benefit from O2, but usually given anyway; hyperventilation as temporary measureC: Prevent HTN, hypotension: altered BP in 1st 24 hours associated with poor outcome; for every 10 over SBP 180, risk of neurological damage increases 40% and poor outcome increases 23%D: Prevent hyper/hypoglycaemia, fever, hypoxia; mannitolSupportive: hydration, nutrition, seizure control (routine anticonvulsants not recommended); pressure care; IDC if unable to void; antiemetic00ED stroke and TIA care bundle: rapid initial stroke screen; ABCD2 if TIA; urgent CT/MRI; NBM until swallow assessed; aspirin as soon as ICH excluded; monitor neurological status, BSL, BP, hydration statusStroke units: single most important recommendation in stroke by National Stroke Foundation; significantly decrease death and disability, more adherance to key principles, more patients eligible for stroke unit than thrombolysis so more impact; interdisciplinary team, early mobilisation, avoid bed rest, active encouragementA: may not be suitable for ETT; elevate head of bed 30 degreesB: no clear benefit from O2, but usually given anyway; hyperventilation as temporary measureC: Prevent HTN, hypotension: altered BP in 1st 24 hours associated with poor outcome; for every 10 over SBP 180, risk of neurological damage increases 40% and poor outcome increases 23%D: Prevent hyper/hypoglycaemia, fever, hypoxia; mannitolSupportive: hydration, nutrition, seizure control (routine anticonvulsants not recommended); pressure care; IDC if unable to void; antiemetic298450497840Complications00Complications1604645497205Cerebral oedema, increased intracranial pressure, haemorrhagic transformation, seizures; in cerebellar, may get rapid deterioration due to oedema, and risk of obstructing hydrocephalus00Cerebral oedema, increased intracranial pressure, haemorrhagic transformation, seizures; in cerebellar, may get rapid deterioration due to oedema, and risk of obstructing hydrocephalus300355486410Management00Management15944856290310Haem-orrhagic CVA00Haem-orrhagic CVA24517356290310BP: reduces haematoma volume; less hazards in reducing as less ischaemic penumbra Lower BP if >200/>120 or MAP >150 aim BP 160/90 or MAP 110, CPP 60-80 (if normal intracranial pressure) Use labetalol 10-20mg IV over 1-2 minutes repeat or double dose at 10 minutes (to max 300mg); also sodium nitroprusside 0.5-10mcg/kg/min, GTNCoagulopathy: increased INR give PTX, FFP If on aspirin and surgery planned give platelets Factor VII not recommended (decreases ICH size but no change in outcome)Indications for ICP monitoring: GCS <8; clinical evidence of transtentorial herniation; significant intraventricular haemorrhage or hydrocephalusIndications for surgery: immediate craniotomy vs delayed evacuation at 5/7 <1cm from surface + <60yrs Hydrocephalus or marked mass effect Cerebellar haemorrhage >3cm (cerebellar is surgical emergency)Indications for intraventricular drain: if blood in ventricles00BP: reduces haematoma volume; less hazards in reducing as less ischaemic penumbra Lower BP if >200/>120 or MAP >150 aim BP 160/90 or MAP 110, CPP 60-80 (if normal intracranial pressure) Use labetalol 10-20mg IV over 1-2 minutes repeat or double dose at 10 minutes (to max 300mg); also sodium nitroprusside 0.5-10mcg/kg/min, GTNCoagulopathy: increased INR give PTX, FFP If on aspirin and surgery planned give platelets Factor VII not recommended (decreases ICH size but no change in outcome)Indications for ICP monitoring: GCS <8; clinical evidence of transtentorial herniation; significant intraventricular haemorrhage or hydrocephalusIndications for surgery: immediate craniotomy vs delayed evacuation at 5/7 <1cm from surface + <60yrs Hydrocephalus or marked mass effect Cerebellar haemorrhage >3cm (cerebellar is surgical emergency)Indications for intraventricular drain: if blood in ventricles1594485487045Ischaemic CVA00Ischaemic CVA2451735487045NINDS: sponsored by industry; multi-centre RCT; tPA vs placebo comparing NIHSS scores and mortality, and probability of favourable outcome, 600 patients; poorly matched groups (less severe stroke in tPA group) corrected for in statistics; 50% patients were treated <90mins which is unrealistic; no control over post-thrombolytic treatment (eg. Stroke unit); no comparison of medians of NIHSS published (?on purpose); decreased efficacy of tPA with time (benefit if <3hrs); 45% were cardioembolic which is abnormally high; showed no improvement at 24hrs, but improved outcome at 3-12/12 (OR 1.7); 13% absolute increase in minimal / no disability (NNT 8); decreased number of patients who are dead or dependent at end of follow up; 2% decreased mortality ( (3/12 mortality 17% in tPA vs 21% in placebo); 6% ICH in tPA (0.6% in placebo) of which 50% were fatal); 3% mortality risk overall (vs 1% in MI) from ICH; increased risk of ICH if >80 years / severe CVAECASS: sponsored by industry; multi-centre RCT; well matched; tPA vs placebo; <6hrs; 600 patients; post-hoc analysis of <3hr group; non-significant improvement of all outcomes with tPA; mortality if major early infarct on CT with tPA 48%; increased haemorrhage with tPA (27% with tPA, 17% with placebo); significant increased mortality with tPAECASS II: sponsored by industry; multi-centre RCT; tPA vs placebo; <6hrs; 800 patients; no statistically significant change in outcome at 90/7 or mortality at 30/7 and 90/7; tPA patients more independent at 90/7; tPA have more ICH and cerebral oedemaECASS III: sponsored by industry; multi-centre RCT; tpA vs placebo; 3-4.5hrs; exclude severe stroke; better modified Rankin/NIHSS score at 90/7 in tPA group (approx. 50% vs 45%); lower mortality at 90/7 in tPA (7.7% vs 8.4%); no change in Barthel Index / Glasgow Outcome score; increased ICH in tPA (27% vs 17%)Interventional radiology: if large vessel occlusion (especially basilar artery / ICA / M1) + few morbidities and good prognosis, and <5hrs; tPA poorly effective in large vessel lesionsIntra-arterial thrombolysis: emerging; treatment window >6hrs; decreased dose of drugs; possibility of mechanical clot disruptionHeparin: if CVA with proven cardioembolic source00NINDS: sponsored by industry; multi-centre RCT; tPA vs placebo comparing NIHSS scores and mortality, and probability of favourable outcome, 600 patients; poorly matched groups (less severe stroke in tPA group) corrected for in statistics; 50% patients were treated <90mins which is unrealistic; no control over post-thrombolytic treatment (eg. Stroke unit); no comparison of medians of NIHSS published (?on purpose); decreased efficacy of tPA with time (benefit if <3hrs); 45% were cardioembolic which is abnormally high; showed no improvement at 24hrs, but improved outcome at 3-12/12 (OR 1.7); 13% absolute increase in minimal / no disability (NNT 8); decreased number of patients who are dead or dependent at end of follow up; 2% decreased mortality ( (3/12 mortality 17% in tPA vs 21% in placebo); 6% ICH in tPA (0.6% in placebo) of which 50% were fatal); 3% mortality risk overall (vs 1% in MI) from ICH; increased risk of ICH if >80 years / severe CVAECASS: sponsored by industry; multi-centre RCT; well matched; tPA vs placebo; <6hrs; 600 patients; post-hoc analysis of <3hr group; non-significant improvement of all outcomes with tPA; mortality if major early infarct on CT with tPA 48%; increased haemorrhage with tPA (27% with tPA, 17% with placebo); significant increased mortality with tPAECASS II: sponsored by industry; multi-centre RCT; tPA vs placebo; <6hrs; 800 patients; no statistically significant change in outcome at 90/7 or mortality at 30/7 and 90/7; tPA patients more independent at 90/7; tPA have more ICH and cerebral oedemaECASS III: sponsored by industry; multi-centre RCT; tpA vs placebo; 3-4.5hrs; exclude severe stroke; better modified Rankin/NIHSS score at 90/7 in tPA group (approx. 50% vs 45%); lower mortality at 90/7 in tPA (7.7% vs 8.4%); no change in Barthel Index / Glasgow Outcome score; increased ICH in tPA (27% vs 17%)Interventional radiology: if large vessel occlusion (especially basilar artery / ICA / M1) + few morbidities and good prognosis, and <5hrs; tPA poorly effective in large vessel lesionsIntra-arterial thrombolysis: emerging; treatment window >6hrs; decreased dose of drugs; possibility of mechanical clot disruptionHeparin: if CVA with proven cardioembolic source379729293814500452755638810PreventionPost-TIA00PreventionPost-TIA1751330627380Anti-platelet agents: CAST and IST trials confirmed aspirin benefit; decreased risk of stroke by 20-30% (50% benefit in 1st 2/52) Clopidogrel + aspirin/dipyridamole may be more effective than aspirin alone, decreased vascular events in patients with AFAnticoagulation: reduces recurrence if AF; warfarin decreases risk of CVA by 2/3 in AF; aim INR 2-3; no benefit if no AF; use aspirin if warfarin contraindicatedBP control: decreased risk of recurrence by 4% after acute stageSmoking: 66% RR reductionCarotid endarterectomy: good if symptomatic; if >80% stenosis, 50% decreased RR of disabling CVA/death; if 70-80% stenosis, 25% decreased RR; no benefit with lesser stenosis; <6% risk of post- op CVA; operate if >70% and symptomatic00Anti-platelet agents: CAST and IST trials confirmed aspirin benefit; decreased risk of stroke by 20-30% (50% benefit in 1st 2/52) Clopidogrel + aspirin/dipyridamole may be more effective than aspirin alone, decreased vascular events in patients with AFAnticoagulation: reduces recurrence if AF; warfarin decreases risk of CVA by 2/3 in AF; aim INR 2-3; no benefit if no AF; use aspirin if warfarin contraindicatedBP control: decreased risk of recurrence by 4% after acute stageSmoking: 66% RR reductionCarotid endarterectomy: good if symptomatic; if >80% stenosis, 50% decreased RR of disabling CVA/death; if 70-80% stenosis, 25% decreased RR; no benefit with lesser stenosis; <6% risk of post- op CVA; operate if >70% and symptomatic ................
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