Improvingedcaredotorg.files.wordpress.com
CVAEpidemiologyTIA: early Ix 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 disabilityDefinitionTIA: FND lasting <24hrs or “a brief episode of neuro dysfunction cause 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 eventPatho-physiology964565140970Brain 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 infarctRisk factors1Y prevention: HTN most important RF; also DM, smoking, incr chol, AF, endocarditis, MS, prosthetic heart valves, male, incr age, heart diseaseICH: HTN (DBP >95), XS ETOH, aneurysm, anticoagulation, cocaine, intracranial SOL, amyloid angiopathySCA most common cause of CVA in childrenCauseThromboembolism is most common at bifurcation of ICA; atherosclerosis most common at origin of ICATIA: below + inflamm; hyperviscosity; subclavian steal; sympathomimeticsCVA: 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 in TIA; more commonly present on activity) 5% atherosclerotic (more commonly present on awakening) Gas embolism, dissection (10-25% CVA’s in young/middle aged), hypotension/perfusion (causes CVA in watershed area) 60% infarcts are haemorrhagic 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 and COW haemorrhage that evolves over few mins will be central location on CT 10-20% are 2Y 50% due to AVM, aneurysms, bleeding diathesis, lesion (eg. Ca), extension of SAH 50% idiopathic lobar haem have rapid onset Sx with focal headache more likely to be peripheral location on CTAssessmentSx TIA: usually last 2-15mins, rarely >1hr; sudden onset without warning, max in minsOE 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; high risk lesion if diastolic componentSx ischaemic CVA: 30% LOC (major altered LOC suggests bilaterally hemisphereric / brainstem dysfunction)Anterior Circulation: 80% brain; ICA + ACA + MCA + opthalmic (due to ICA disease; 80% CVA’s are MCA territory) Supplies frontal lobe, parietal lobe, most of temporal lobe (ant/med cortex), optic nerve significant oedema, decr LOC----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------MCA (80%) parietal, some temporal, Broca’s (speaking), Wernickes (understanding)Cause: embolicSx: Contralat hemiplegia (face (UMN pattern) +arm > leg) / sensory loss Eyes deviated towards; contralat homonymous hemianopia L (dominant) aphasia / expressive (ant) or receptive (post) aphasia, agnosia, agraphia, acalculia, L-R disorientation R (non-dominant) L sided neglect spatial neglect, dressing apraxia--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------ACA medial frontal and parietal, basal ganglia, internal capsule, olfactory bulbRare as good collateral from AcommASx: Contral hemiplegia (leg > arm), difficulty initiating mvmt No sensory changes Confusion, personality change Abnormal conjugate gaze Grasp /pout / palmomental reflex, urinary incontinence; gait; smell; sensory / visual inattention L (dominant) speech problems (difficulty initiating) R (non-dominant) confusion, neglect--------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------OpthalmicSx: monoocular visual loss (amourosis fugax)Posterior circulation: 20% brain; vertebral + basilar + PCA Supplies cerebellum, brainstem, thalamus, occipital lobe, some of temporal lobe (medial), auditory and vestibular---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------PCA occipital lobe, some temporalSx: hemisensory loss No motor weakness Honomynous hemianopia, quadrantanopia, cortical blindness (if bilateral) Dyslexia, memory loss Ipsilat III palsy---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------Vertebrobasilar cerebellum, brainstemSx: ataxia, dizziness, N+V, nystagmus, diplopia, vertigo, INO, CN palsies, dysarthria, facial weakness Ipsilat CN signs, contralat body signs Lateral medullary syndrome: Ipsilat UMN Horner’s syndrome, loss of pain and T sensation in face inc loss of corneal reflex = Wallenberg’s Contralat loss of pain and T in body (spinothalamic tract) Dysphagia, dysarthria, dysphonia (IX, X affected) Conjugate gaze palsy, vertigo, nystagmus, ataxia, dysarthria, dysphagia---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------Locked in syndrome: basilar arteryLacunar basal ganglia, pons, cerebellum, ant internal capsule, deep cerebral white matterSx: 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 dysarthriaMng: aspirin less helpful; good prognosisSx haemorrhagic CVA: ICH tends to have more N+V+H; ICH tends to have slow onset; LOC often impaired in ICH; 25% ICH initially alert then deterioriate over 24hrs; high mortality if blood in ventricles Putamen: contralat hemiplegia no sensory loss eyes deviate to contralat side Thalamic: contralat hemiplegia; sensory deficit Eyes down and in, unequal pupils, absent light reflex, ipsilat Horner’s, lat gaze defect Aphasia Pons: quadriplegia; decerebrate rigidity (decorticate is medulla / midbrain) Pinpoint pupils Deep coma, incr RR, HTN, hyperhydrosis Cerebellar: eye deviate to contralat side Vomiting, vertigoDDSeizures (20%; esp in elderly or prev CVA), sepsis (13%), toxic/metabolic (eg. hypoG, drugs, hypoxia, hypoNa; 11%); SOL (9%); syncope (9%)Others: migraine, Ca, SDH, herpes encephalitis, neuropathy, psychogenic, aortic dissectionTIA risk20-25% will have CVA in next 1yr; 30% with TIA will have CVA within 5yrs (5% in 48hrs, 10% in 1/12, 10-20% in 90/7)ABCD2 score: may underestimate risk Age >60yrs (1) (>75yrs in CCFHTNAgeDMSX2) 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 = 1% 2/7, up to 15% 7/7 <4 do CT head and carotid USS within 48-72hrs; OP FU 4-5 = mod = 4% 2/7, 20-25% 7/7 6-7 = high = 8% 2/7, 25-30% 7/7 >4 admit; do CT/MRI within 24hrsABCD score: 2-5% 7/7 risk if <5, 35-55% if 6California score: age, DM, duration of Sx, weakness, speech impairmentStroke screening toolsROSIER 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, sens 90-95%, spec 75-90% for stroke unlikelyFAST: facial mvmt, arm mvmt, speech, testPros: used pre-hospital to allow patients to be taken to stroke centresOthers: CPSS, LAPSS, MASSStroke assessment scalesNIH stroke scale: Pros: quick, reproducible, correlates with infarct volume, measures level of impairment; allows comparison of deficit over timeCons: weighted towards ant circulationInvestigationBloods: electrolytes, BSL, FBC; ABGs if resp depression; ESR if vasculitis suspected or age <40yrsECG: arrhythmia, MI; AF most common in TIACXR: exclude aortic dissection, aspiration, intrathoracic CaCT head: In TIA / CVA: low yield in TIA; if infarct, no abnormality in 1st few hours (sens 50% at 6hrs, spec >95%) Early changes suggest large infarct (loss of grey-white differentiation is 1st sign, parenchymal hypodensity, effacement of sulci, V compression, local mass effect, loss of insular ribbon, obscuration of lentiform nucleus, hyperdense MCA or other (100% spec, 30% sens for MCA) incr attentuation (for few wks) decr attenuation with mass effect and ill defined margins isodense at 1-2/52 more decr attenuation looks like CSF at few mnths 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 oedemaIn ICH: incr attenuation in 1st wk (hypodense area may be active bleeding) decr density and blurring of margins from periphery after 1/52 surrounding oedema (may contrast enhance mimicking Ca) loss of mass effect isodense at 3/52 hypoattentuation at 10/52 little residual change; rpt in 24hrs will show incr in haematoma size in 30% (assoc 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 1-2hrs, 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 haemorrhageMRA: 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 resolutionMRI: more sens (esp in post territory / brainstem CVA; and for ICH >1/52 from onset), but may delay trts; less widely availableDiffusion MRI: can detect ischaemia within 2hrs; 75% sens in 3hrs, >95% sens >3hrs, >95% specPerfusion MRI: diffusion-perfusion mismatch idenitifies salvageable penumbra and can more accurately 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% sens, 90% spec for >70% stenosisEcho: if evidence of sturctural cardiac disease OE/ECG/CXR, or suspect emboli (eg. AF, recent MI); low yield otherwiseHolter: if no other cause for TIA foundComplicationsCerebral oedema, incr ICP, haemorrhagic transformation, seizures; in cerebellar, may get rapid deterioration due to oedema, and risk of obstructing hydrocephalusMngED 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 statusStroke units: single most important recommendation in stroke by National Stroke Foundation; significantly decr 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 30degB: no clear benefit from O2, but usually given anyway; hyperventilation as temporary measureC: Prevent HTN, hypotension: altered BP in 1st 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; mannitolSupportive: hydration, nutrition, seizure control (routine anticonvulsants not recommended); p care; IDC if unable to void; antiemeticMng of CVABP CVA: aggressive BP lowering may decr cerebral perfusion and worsen stroke Sx lower BP if consistently >220 / >120-140, or MAP >130 aim 10-15% decr in BP within 24hrs if for thrombolysis need BP <185/110 to meet criteriaAntiplt: commence aspirin (clopidogrel if CI’ed; delay 24hrs if thrombolysed) decr risk of early death and recurrent CVA (Chinese acute stroke trial); beneficial as 2Y prevention No evidence for heparin; Warfarin later if AFThrombolysis: 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 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 or harm (ASK, MAST-I, MAST-E (all used SKA) all ceased early due to incr mortality risk); no data if >80yrs; small no patients studied in few trials (more in MI); patients rarely fit criteria (eg. Time to presentation; ie. 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 24hrs; 75% patients will improve with placebo; unlikely benefit in lacunar syndromes / large vessel occlusion; if used 90-180mins, may incr mortality 1%, if 3-4.5hrs, 1% absolute incr mortality may disrupt care of other patients (inc from post-thrombolyis 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. Trt after 3hrs); difficult work up (easy in MI); short time frame (6hrs in MI); unknown magnitude of trt effect, duration of therapeutic window, which patients will benefit 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 who are 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); signficant 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 oedemaInterventional radiology: if large vessel occlusion (esp basilar art / ICA / M1) + few morbidities and good prognosis, and <5hrs; tPA poorly effective in large vessel lesionsIntra-arterial thrombolysis: emerging; trt window >6hrs, decr dose of drugs, possibility of mechanical clot disruptionHeparin: if CVA with proven cardioembolic sourceMng of ICHBP ICH: reduces haematoma vol; less hazards in reducing as less ischaemic penumbra Lower BP if >200 / >120 or MAP >150 aim 160/90 or MAP 110, CPP 60-80 (if normal ICP)Use labetalol 10-20mg IV over 1-2mins repeat or double dose at 10mins (to max 300mg) Na nitroprusside 0.5-10mcg/kg/min or GTNCoagulopathy: incr INR PTX, FFP to normal INR Plts: if on aspirin and OT planned Factor VII decr ICH size but no change in outcome, so not recommendedIndications for ICP monitoring: GCS <8; clinical evidence of transtentorial herniation; significant intraV haem or hydrocephalusIndications 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 interV drain: if blood in V’sAdmit 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 anticoagPreventionPrevention post-TIA: Anti-plt agents: CAST and IST trials confirmed aspirin benefit; decr risk of stroke by 20-30% (50% benefit in 1st 2/52) Clopidogrel + aspirin/dipyridamole may be more effective than aspirin alone, decr vascular events in patients with AFAnticoagulation: 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’edBP control: decr risk of recurrence by 4% after acute stageSmoking: 66% RRRCarotid 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 symptomaticNotes from: DunnSummary of SyndromesSiteMotor changesSensory changesEye changes OtherMCAContralat weakness (face, arm > leg)Contralat sensory lossContralat HHEyes deviated towardsL: aphasia, agnosiaR: spatial neglect, dressing apraxiaACAContralat weakness (leg > arm)No sensory lossAbnormal conjugate gazePersonality, incontinenceL: speechR: neglectPCANoneContralat sensory loss (pinprick and light touch)HH, quadIpsilat III palsy (down + out)Dyslexia, memoryVertebrobasilarIpsilat facial weakness + CN palsies; contralat motor weakness?INO, diplopia, nystagmusAtaxia, N+V, vertigoLat medullary syndromeIpsilat VII, IX, X (Horner’s syndrome)Ipsilat pain and T face, contralat pain and T bodyAbnormal conjugate gaze, nystagmusAtaxia, vertigoDysarthria, dysphasiaWallenburg’s syndromeIpsilat facial weakness, contralat body weaknessIpsilat pain and T face, contralat pain and T body?Cerebellar signsInternal capsuleContralat weakness---Thalamus-Contralat sensory loss--PonsHand clumsiness--DysarthriaPutamenContralat weakness-Eyes deviate away-ThalamusContralat weaknessContralat sensory lossIpsilat Horner’s, lat gaze defect, unequal pupils, absent light reflexAphasiaPonsQuadriplegia, decerebrate-Pinpoint pupilsComa, incr RR, HTN, hyperhydrosisCerebellar--Eyes deviate awayVomiting, vertigo ................
................
In order to avoid copyright disputes, this page is only a partial summary.
To fulfill the demand for quickly locating and searching documents.
It is intelligent file search solution for home and business.
Related download
Related searches
- wordpress passing data between pages
- wordpress business templates
- wordpress rss feed not working
- wordpress jquery is not defined
- create wordpress blog
- wordpress roles editor
- wordpress full rss feed
- wordpress rss feed settings
- wordpress rss feed plugin
- wordpress display rss feed
- wordpress rss feed link
- wordpress rss feed to post