CVA Sept

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Eleanore Parker
5 years ago
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CVA Sept 2014 Epidemiology TIA: early Ix and intervention can prevent 80% early CVA s CVA: 3 rd highest cause of death in developed countries; incidence doubles every decade over 55yrs; variable

1 CVA Sept 2014 Epidemiology TIA: early Ix and intervention can prevent 80% early CVA s CVA: 3 rd 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 home ICH: death 30-50% (50% deaths within 48hrs; >80% if on warfarin); 33% discharge home; 30% 1yr survival; ICH more common in men Lacunar: death low; 30% long term disability Definition TIA: FND lasting <24hrs or a brief episode of neuro dysfunction caused by focal brain/retinal ischaemia with clinical Sx usually lasting <1hr, without evidence of acute infarction Cerebral infarct: thrombotic / embolic occlusion of major intracranial BV; acute non-reversing loss of brain function due to vascular event Pathophysiology Brain 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 stops Ischaemic penumbra: threatened but potentially salvageable brain surrounding infarct Risk factors Primary prevention: HTN most important RF; also DM, smoking, incr chol, AF, endocarditis, MS, prosthetic heart valves, male, incr age, heart disease ICH: HTN (DBP >95), XS ETOH, aneurysm, anticoagulation, cocaine, intracranial SOL, amyloid angiopathy Cause Thromboembolism is most common at bifurcation of ICA; atherosclerosis most common at origin of ICA TIA: below + inflamm; hyperviscosity; subclavian steal; sympathomimetics 75% infarction = 10% death 50% unknown 25% lacunar (due to lipohyalinosis, assoc with DM and HTN) 20% embolic (eg. mural/valve disease; embolisation more common than TIA; more commonly on activity) 5% atherosclerotic (more commonly present on awakening) Gas embolism, dissection (10-25% CVA s in young), hypotension/perfusion (cause CVA in watershed area) 25% haemorrhage = 30-50% death 50% intracerebral (???2x more common than SAH) 50% SAH 80-90% are 1Y (spontaneous rupture of small BV by chronic HTN or amyloid angiopathy) Putamen > thalamus > pons > cerebellum, upper brainstem, basal ganglia HTN - Charcout-Bouchard microaneurysms of penetrating arteries of MCA, basal, COW - haemorrhage evolves over few mins will be central location on CT Locations of intracranial haemorrhages: 1. Hypertensive: putamen, thalamus, pons, cerebellum 2. Amyloid angiopathy: lobar = better prognosis 3. Cerebellar: may be undistinguishable from infarct. Usually rapid decrease in GCS/coning. 1

2 10-20% are secondary 50% due to AVM, aneurysms, bleeding diathesis, lesion (eg. Ca), extension of SAH 50% idiopathic Lobar haemorrhages have rapid onset Sx with focal headache More likely to be peripheral location on CT Assessment Symptoms TIA: Usually last 2-15mins, rarely >1hr; sudden onset without warning, max in mins Examination TIA: Usually normal; look for evidence of cardiac / vascular disease; carotid bruit 75% sens and >75% spec for mod-high grade stenosis; 90% carotid bruits are mod-high degree, 5-10% are surgically amenable Anterior Circulation: 80% brain; ICA + ACA + MCA + ophthalmic Supplies frontal lobe, parietal lobe, most of temporal lobe (ant/med cortex), optic nerve MCA (80%) - parietal, some temporal, Broca s (speaking), Wernickes (understanding) ACA - medial frontal and parietal, basal ganglia, internal capsule, olfactory bulb Rare as good collateral from AcommA Ophthalmic Monocular visual loss (amaurosis fugax) Posterior circulation: 20% brain; vertebral + basilar + PCA Supplies cerebellum, brainstem, thalamus, occipital lobe, temporal lobe (medial), auditory, vestibular PCA - occipital lobe, some temporal Vertebrobasilar - cerebellum, brainstem Locked in syndrome: basilar artery Lacunar - basal ganglia, pons, cerebellum, ant internal capsule, deep cerebral white matter Localised sensory/motor defects (eg. pure sensory, pure motor, clumsy hand) Internal capsule - contralat motor loss, no sensory loss Thalamus/pons - sensory loss, no motor weakness Pons - hand clumsiness and dysarthria Management: aspirin less helpful; good prognosis Symptoms haemorrhagic CVA: ICH tends to have more N+V+H; slow onset; LOC often impaired; 25% initially alert then deterioriate High mortality if blood in ventricles Differential diagnosis Seizures (20%; esp in elderly or prev CVA) Sepsis (13%) Toxic/metabolic (eg. hypoglycaemia, drugs, hypoxia, hypona; 11%) SOL (9%) Syncope (9%) Others: migraine, Ca, SDH, herpes encephalitis, neuropathy, psychogenic, aortic dissection 2

3 Site Motor Sensory Eye Other MCA Contralat weakness (face, arm> leg) Contralateral sensory loss Contralat HH, eyes deviated towards L: aphasia, agnosis R: spatial neglect ACA Contralat weakness (leg>arm) None Abnormal conjugate gaze Personality, incont L: speech R: neglect PCA None Contralat loss pinprick/light touch HH, ipsilateral III palsy (down/out) Dyslexia, memory Vertebrobasilar Ipsilat facial weakness/cn palsies; contralat motor weakness INO, diplopia, nystagmus Ataxia, N+V, vertigo Lat medullary syndrome Ipsilat VII, IX, X (Horner s syndrome) Ipsilat pain and T face, contralat pain and T body Abnormal conjugate gaze, nystagmus Ataxia, vertigo, dysarthria, dysphasia Wallenburg s syndrome Ipsilat facial weakness, contralat body weakness Ipsilat pain and T face, contralat pain /T body Cerebellar signs TIA risk 20-25% will have CVA in next 1yr 30% in next 5 years 5% in 48hrs, 10% in 1/12, 10-20% in 90/7 ABCD2 score: may underestimate risk Age >60yrs (1) BP >140/90 (1) Clinical features: unilateral weakness (2)/speech impairment without weakness (1) Duration: >60mins (2)/10-60mins(1) DM (1) 0-3 = low, 4-5 = mod, 6-7 = high <4 - do CT head and carotid USS within 48-72hrs; OP FU >4 - admit; do CT/MRI within 24hrs 2-5% 7/7 risk if <5, 35-55% if 6 Stroke screening tools ROSIER scale: GCS, BP, BSL, LOC/syncope, seizure, facial/arm/leg weakness, speech, visual field defect Pros: validated specifically for ED after triage; recommended by NICS, NSF, NICE, SIGN; if score <0, sens 90-95%, spec 75-90% for stroke unlikely FAST: facial movement, arm movement, speech, test Pros: used pre-hospital to allow patients to be taken to stroke centres NIH stroke assessment scale Pros: quick, reproducible, correlates with infarct volume, measures level of impairment; allows comparison of deficit over time. Cons: weighted towards ant circulation 3

4 Investigation Bloods: electrolytes, BSL, FBC; ABGs if resp depression; ESR if vasculitis suspected or age <40yrs ECG: arrhythmia, MI; AF most common in TIA CXR: exclude aortic dissection, aspiration, intrathoracic Ca CT head: In TIA / CVA: low yield in TIA; if infarct, no abnormality in 1 st few hours (sens 50% at 6hrs, spec >95%) Early changes suggest large infarct (loss of grey-white differentiation 1 st sign, parenchymal hypodensity, effacement of sulci, ventricle compression, local mass effect, loss of insular ribbon, obscuration of lentiform nucleus, hyperdense MCA or other (100% spec, 30% sens for MCA) Poor outcome with thrombolysis if: hypodensity >1/3 MCA territory (19% fatal haem vs 0%; 7% good 3/12 outcome vs 17%), sulcal effacement, mass effect, cerebral oedema ASPECTS: CT score for use in MCA CVA; score <7 predicts worse functional outcome at 3/12 and symptomatic haemorrhage 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 1-2hrs, only takes a few mins, will show potentially reversible penumbra, may need double contrast bolus dose; esp do if peripheral ICH to determine source of haemorrhage MRA: 80% sens, 95% spec 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 resolution MRI: more sens (esp in post territory/brainstem CVA; and for ICH >1/52 from onset), but may delay trts; less widely available Transcranial Doppler USS: rapid, but need expertise; can assess MCA Carotid Doppler USS: do if suspected ant circulation TIA; 85% sens, 90% spec for >70% stenosis Echo: if evidence of structural cardiac disease, or suspect emboli (eg. AF, recent MI); low yield otherwise Holter: if no other cause for TIA found Complications Cerebral oedema, incr ICP, haemorrhagic transformation, seizures Cerebellar - may get rapid deterioration due to oedema, and risk of obstructing hydrocephalus Management ED 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 NS, BSL, BP, hydration status Stroke units: single most important recommendation in stroke by National Stroke Foundation; significantly decr death and disability, more adherence to key principles, more patients eligible for stroke unit than thrombolysis so more impact; interdisciplinary team, early mobilisation, avoid bed rest, active encouragement A: may not be suitable for ETT; elevate head of bed 30deg B: no clear benefit from O2, but usually given anyway; hyperventilation as temporary measure C: Prevent HTN, hypotension: altered BP in 1 st 24hrs assoc with poor outcome; for every 10 over SBP 180, risk of neuro damage incr 40% and poor outcome incr 23% D: Prevent hyperg/hypog, fever, hypoxia; mannitol Supportive: hydration, nutrition, seizure control (routine anticonvulsants not recommended); pressure cares; IDC if unable to void; antiemetic 4

5 Management of CVA BP Aggressive BP lowering may decrease cerebral perfusion and worsen stroke Sx Lower BP if consistently >220 / > , or MAP >130 Aim 10-15% decr in BP within 24hrs If for thrombolysis need BP <185/110 to meet criteria Antiplatelet Aspirin (clopidogrel if CI ed; delay 24hrs if thrombolysed) Decr risk of early death and recurrent CVA (Chinese acute stroke trial); beneficial as secondary prevention No evidence for heparin; Warfarin later if AF Thrombolysis To salvage penumbra if commenced within <3 hrs Dose: 0.9mg/kg tpa (max 90mg), 10% as bolus, 90% over 60mins Admit stroke unit/hdu bed check BP Q15min for 2hrs - Q30mins for 6hrs - Q1hr for 16hrs CI s: unknown time of onset; improving Sx; minor (NIHSS <4); major (NIHSS >25); SBP >185; DBP >110; high risk CT findings (>1/3 MCA territory, multilobar infarction); seizure; plt <100; PT >15; BSL <2.7 / >22.2; Sx suggestive of SAH; heparin in last 48hrs, incr APTT; unable to consent; >3hrs; >80yrs; demonstrable perfusion Pros: benefits at 3-12/12; NNT 8; if used <90mins NNT 4.5 if mins, 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 NINDS: 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 trt (eg. Stroke unit); no comparison of medians of NIHSS published (?on purpose); decr 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 incr in minimal/no disability (NNT 8) decr no patients dead or dependent at end of FU 2% decr 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 - incr risk ICH if >80yrs / severe CVA ECASS III: sponsored by industry; multi-centre RCT; tpa vs placebo; 3-4.5hrs; excluded 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 Incr ICH in tpa (27% vs 17%) ECASS: 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%; incr haem with tpa (27% with tpa, 17% with placebo); significant incr mortality with tpa ECASS 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 oedema 5

6 Interventional radiology: if large vessel occlusion (esp basilar art / ICA / M1) + few morbidities and good prognosis, and <5hrs; tpa poorly effective in large vessel lesions Intra-arterial thrombolysis: emerging; trt window >6hrs, decr dose of drugs, possibility of mechanical clot disruption Heparin: if CVA with proven cardioembolic source Management of ICH BP Control Reduces haematoma volume; less hazards in reducing as less ischaemic penumbra Lower BP if: >200 / >120 or MAP >150 Aim 160/90 or MAP 110, CPP (if normal ICP) Labetalol 10-20mg IV over 1-2mins - repeat or double dose at 10mins (to max 300mg) or Sodium nitroprusside mcg/kg/min or GTN Coagulopathy Incr INR - give PTX, FFP Platelets - if on aspirin and OT planned Factor VII - decreases ICH size but no change in outcome, so not recommended Indications for ICP monitoring GCS <8 Clinical evidence of transtentorial herniation Significant intraventricular haemorrhage or hydrocephalus Indications for OT Immediate craniotomy vs delayed evacuation at 5/7 <1cm from surface + <60yrs Hydrocephalus or marked mass effect Cerebellar haem >3cm (Cerebellar is surgical emergency) Indications for intraventricular drain Blood in ventricles Admit TIA if: ABCD2 score >4; 4 TIA s in 2/52; 3 TIAs in 72hrs; 2 TIA s in 24hrs; high grade carotid stenosis;?cardiac source; embolic TIA despite anticoag Prevention Prevention post-tia: Anti-plt agents: CAST and IST trials confirmed aspirin benefit; decr risk stroke 20-30% (50% benefit in 1 st 2/52) Clopidogrel + aspirin/dipyridamole may be more effective than aspirin alone, decr vascular events in AF Anticoagulation: reduces recurrence if AF; warfarin decr risk of CVA by 2/3 in AF; aim INR 2-3; no benefit if no AF; use aspirin if warfarin CI ed BP control: decr risk of recurrence by 4% after acute stage Smoking: 66% RRR Carotid endarterectomy: good if symptomatic; if >80% stenosis, 50% decr RR of disabling CVA/death; if 70-80% stenosis, 25% decr RR; no benefit with lesser stenosis; <6% risk of post-op CVA; operate if >70% and symptomatic 6

Stroke/TIA. Tom Bedwell

Stroke/TIA. Tom Bedwell Stroke/TIA Tom Bedwell tab1g11@soton.ac.uk The Plan Definitions Anatomy Recap Aetiology Pathology Syndromes Brocas / Wernickes Investigations Management Prevention & Prognosis TIAs Key Definitions Transient