Stroke management protocol

Stroke Management Protocol

Acute Stroke: Management ProtocolDr. Varun KatariaM.D., D.M.(Neurology)Ex-Asst. Professor, C.M.C. VelloreConsultant Neurologist, Medanta Superspeciality Hospital, Indore

Case-145 yrs old gentleman with h/o Diabetes presented to our ER at 9pm with Acute onset slurring of speech which started 1 hour back. No h/o seizures, LOC. On examination, his GCS was E4V4M6. Facial weakness on right side with right pronator drift. His NIHSS 4.

B.P.- 170/90mmHg, NSR, RBS 167mg%, SpO2-95% at room air.

9:30pm - Brain Scan

10pm - He was taken up for IV Thrombolysis with Actilyse (rtPA)BW-67kgDose required 0.9 * 67 = 60.36mg bolus f/b 54mg infusion over 1 hour with B.P. monitoring.Heparin or Aspirin was NOT given for 24 hours.

Next day 10am Repeat Scan

Antiplatelets, Statins were started.Planned for Echo, Carotid doppler and serum homocysteine

After 2 days was discharged with mild clumsiness on right side and slurred speech.

SO WHAT?

Stroke is the first leading cause of disability and 3rd leading cause of mortality

Prevalence rate of stroke - 84-262/100,000 in rural and 334-424/100,000 in urban areas Incidence rate is 119-145/100,000 Case fatality rates - upto 42% (Kolkata)

0.63 mil. deaths

Stroke Epidemiology and Stroke Care Services in IndiaJeyaraj Pandian, Paulin SudhanJ Stroke. Sep 2013; 15(3): 128134

Three Stroke Types

IschemicStroke

Clot occludingartery85%

Intracerebral Hemorrhage

Bleedinginto brain10%

Subarachnoid Hemorrhage

Bleeding around brain5%

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TIA v/s STROKETIA is a brief episode of neurological dysfunction caused by a focal disturbance of brain or retinal ischemia, which clinical symptoms typically lasting less than 60 minutes and without evidence of infarctionSTROKE any neurological dysfunction caused by a focal disturbance of brain or retinal ischemia lasting longer than 60 minutes with radiological evidence of infarction.

Mr. Sharma, 47yr old male, Presented with acute heavyness and numbness of right upperlimb and face on 11/9/15 at 10:30am in morning. He went to a local doc who found his B.P. to be 190/110 mmHg.

He was referred to us. At 11:15am, his B.P. was 170/100 mmHg and was asymptomatic. The relative accompanying said that his speech was little different from before.

Stroke protocol Scan Combination of plain CT brain with DWI/ADC and FLAIR.

Scan Normal.Kept under observation for 1 day. Diagnosis TIA (Anterior Circulation Possibly Left MCA)

Treatment Ecosprin 150mg 2 tab stat, Statins, Antihypertensives to keep B.P. at 140/90 mmHg.

CT of brain w/o contrastEarly signs of ischemic stroke:Hyper-dense vessel signLoss of insular ribbonObscuration of lenticular nucleusLoss of gray-white matter distinctionSulcal effacementAreas of hypo-attenuation

EXCLUSION CRITERIA AREAbsolute - Presence of intracranial bleedMultilobar infarction with well defined hypodensity in > 1/3 of vascularterritory

RECOMMENDATIONS FOR PATIENTS WITH SYMPTOMS OF AIS THAT HAVE RESOLVEDNon invasive imaging of cervical vessels

CTA or MRA of intracranial vasculature to exclude the presence of proximal intracranial stenosis or oclussio. Confirmation with catheter angiography is recommended.

PATIENTS WITH TIA SHOULD UNDERGO NEUROIMAGING EVALUATION WITHIN 24 HOURS FROM SYMPTOMS ONSET

UNCHANGED FROM 2009

Acute Ischemic Stroke

What is acute stroke?An ischemic stroke is the result of a vascular occlusion in the blood supply to an area of the brain, which results in cerebral ischemia.

CAUSES (ETIOLOGIES) OF ISCHEMIC STROKE:SIX MAIN CATEGORIES

Hypercoagulablestates

NonatheroscleroticvasculopathiesYOUNGER PATIENTS(< 55)Correct therapy depends on cause of stroke!Cause & risk factor are not synonymousmust Rx both!

Large-arteryatherosclerosis

Small-arterydiseaseOLDER PATIENTS(> 55)CardioembolismHypotension

ETIOLOGIC EVALUATION:IDENTIFY STROKE, FIND SOURCE OF CLOTINVASIVEDay 2*Catheterangiogram*TEENONINVASIVEDay 1ARTERIESHEARTBLOODECG & monitorCardiac biomarkersTransthoracic echo (TTE)MRI & intracranial MRACarotid duplex (CD)*Hypercoagulable profile*in selectpatients

Acute (4 hours)InfarctionSubtle blurring of gray-white junction & sulcal effacementSubacute (4 days) InfarctionObvious dark changes & mass effect (e.g., ventricle compression)

R

RLL

ISCHEMIC STROKE PATHOPHYSIOLOGYThe First Few Hours

PenumbraCore

Clot in Artery

TIME IS BRAIN:SAVE THE PENUMBRA

Penumbra is zone of reversible ischemia around core of irreversible infarctionsalvageable in first few hours afterischemic stroke onset

Penumbra damaged by: Hypoperfusion Hyperglycemia Fever Seizure

ISCHEMIC PENUMBRA: PATHOPHYSIOLOGYOF THERAPEUTIC WINDOW

PenumbraCore

CEREBRALBLOODFLOW(ml/100g/min) CBF< 8CBF8-18TIME (hours)123201510 5

PENUMBRA

CORENeuronal dysfunctionNeuronal deathNormal functionIdentification of penumbra through MRI perfusion-diffusion mismatch or perfusion CT may replace time as the major indication for emergency acute ischemic stroke therapies.

Potential to Reverse Neurologic Impairment With Thrombolytic ReperfusionSaver. Stroke 2006;37:263-266.Gonzlez. Am J Neuroradiol 2006;27:728-735.Donnan. Lancet Neurol 2002;1:417-425.

An untreated patient loses approximately 1.9 million neurons every minute in the ischemic areaReperfusion offers the potential to reduce the extent of ischemic injuryIschaemic core(brain tissue destined to die)Penumbra (salvageable brain area)

32Speaker Notes:

Reperfusion may play role in reducing the extent of the ischaemic injury.Umbra (dead tissue) or damaged part will not be able to recover fully. Penumbra(salvagable tissue) is the area which will potentially benefit from timely thrombolysis treatment.

Prehospital management of potential stroke patientsRecommendedAssess & manage ABCInitiate cardiac monitoringSupplement O2 to maintain O2 saturation > 94%Establish IV accessDetermine blood glucose and treat accordingly

33ASA Guidelines. Stroke 2013

Prehospital management of potential stroke patientsRecommendedDetermine time of symptom onset or last known normalRapidly transport patient to nearest most appropriate hospitalNotify hospital of pending stroke patient arrival


Prehospital management of potential stroke patientsNot RecommendedDo not initial interventions for HT unless directed by medical commandDo not administer excess IV fluids Do not administer dextrose containing fluids in non-hypoglycemic patients


Prehospital management of potential stroke patientsNot RecommendedDo not administer medications by mouth (maintain NPO)Do not delay transport for prehospital interventions


Acute ischemic strokeGeneral managementAirway, Breathing, CirculationFeverBlood glucoseHypertensionIV fluidTreatment of underlying diseases37

THE AIS-BP RELATIONSHIPIn AIS, high BP is a response,not a causedont lower it!BP increase is due to arterial occlusion (i.e., an effort to perfuse penumbra)Failure to recanalize (w/ or w/o thrombolytic therapy) results in high BP and poor neuro outcomesLowering BP starves penumbra, worsens outcomes

PenumbraCore

Clot in Artery

AIS IS NOT A HYPERTENSIVE EMERGENCY!ASA/AHA AIS Guidelines tables no longer include recs for BP Rx in non t-PA patients

Text of guidelines state Do not Rx unless BP > 220/120, but also state:No data to suggest 220/120 is dangerous & requires RxEvidence that BP lowering worsens outcomes is concerningGoal is to avoid overtreating pts until definitive data available

Only definite indications to BP emergently in AIS:AMI, CHF, Ao dissection, ARF, or HTN encephalopathyCandidate for thrombolysis and BP > 185/110

MAY LOWER BP SLIGHTLY PRE T-PAMUST PICK AN UPPER LIMIT TO TREAT220/120 IS ONE OPTIONIf all t-PA criteria met except sustained BP > 185/110:

Ensure 2 IVs (NS @ 75 cc/h, saline lock)Calm patient, empty bladderRecheck BP, lower slightly if necessary

SBP > 185 and < 220 orDBP > 110 and < 120

Avoid excessive lowering of BP just to give t-PADont kill the penumbra to save the penumbra

Lower BPpre-t-PA

Acute specific treatmentRecanalization IV rt-PA

Neuroprotective treatmentAspirin in first 48 hoursAnticoagulant

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NIHSS cont.NIHSS Interpretation

Stroke ScaleStroke Severity0No Stroke1-4Minor Stroke5-15Moderate Stroke15-20Moderate/Severe Stroke21-42Severe Stroke

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NIHSS and Outcome Prediction

NIHSS below 12-14 will have an 80% good or excellent outcome

NIHSS above 20-26 will have less than a 20% good or excellent outcome

Lacunar infarct patients had the best outcomes

Adams HP Neurology 1999;53:126-131Baseline NIH Stroke Scale score strongly predicts outcome after stroke (TOAST)

Study done by Adams and his colleagues used the Barthel Index (BI) and the Glasgow Outcome Scale (GOS) to assess over 1200 patients outcomes at 7 days and 3 months.

Between 70% and 80% of patients who have suffered a lacunar stroke are functionally independent at 1 year, compared with fewer than 50% of patients who have had a nonlacunar stroke. 44

Case 3 85 year old male who woke up with left face, arm, and leg numbness

History of HTN, DM, and tobacco use

Meds: Insulin, aspirin

Case 3BP- 168/96, P 92

General exam: Unremarkable

NEURO EXAM:- Decreased sensation on left face, arm, and leg

Case 3

Case 3

Right thalamic lacunar infarct

Not a candidate for intervention

Discharged to rehab 72 hours after admission

Acute ischemic stroke

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Intravenous thrombolysis

FDA approved 1996 based on NINDS rt-PA Stroke Study

Treatment within 3 hours of symptom onset

Complete neurological improvement or improvement >= 4 points on NIHSS at 24 hoursComplete or nearly complete recovery at 3 months

Symptomatic brain hemorrhage is major risk (6.4% VS 0.6%)

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AIS EMERGENCY THERAPY: IV TISSUE PLASMINOGEN ACTIVATOR (T-PA)< 3.0 HoursNo upper age limitNo limit on stroke sizeCan give if taking warfarin & INR < 1.73.0-4.5 HoursDo NOT give if:Pt > 80 yoNIHSS > 25DM w/ previous strokeTaking warfarin at all Must give < 4.5 hearlier you give it, better the outcome Stroke onset = last time known to be normal Do NOT give if glucose < 50 Do NOT give if BP > 185/110 Disability risk 30% despite ~5% symptomatic ICH risk Lawsuits for not giving >>> lawsuits for giving

Patients with ischemic stroke within 4.5 hours who could be treated with rt-PA

Inclusion criteriaMeasurable neurological deficitOnset of symptoms < 4.5 hoursAge 18 years



Exclusion criteriaSignificant head trauma or prior stroke in previous 3 monthsSymptoms suggest SAHArterial puncture at non compressible site in previous 7 daysHistory of previous intracranial hemorrhageIntracranial neoplasm, AVM, or aneurysmRecent intracranial or intraspinal surgery



Exclusion criteriaElevated BP (systolic > 185 or diastolic >110 mmHg)Active internal bleedingAcute bleeding diathesis, including but not limited to platelet < 100,000 /mm3Heparin received within 48 hours, resulting in elevated aPTTCurrent use of anticoagulant with INR > 1.7



Exclusion criteriaCurrent use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated sensitive laboratory tests (ie. aPTT, INR, platelet count, ECT, TT or appropriate factor Xa activity assay)Blood glucose concentration < 50 mg%CT shows multilobar infarction (hypodensity > 1/3 cerebral hemisphere)



Relative exclusion criteria*Only minor or rapid improving stroke symptomsPregnancySeizure at onsetMajor surgery or serious trauma within previous 14 daysRecent GI or Urinary tract hemorrhage within previous 21 daysRecent acute MI within previous 3 months56ASA Guidelines. Stroke 2013*Patients may received rtPA despite 1 or more relative contraindication, consider risk to benefit carefully

Ancillary TestingBlood glucose Electrolytes Complete blood count PT (prothrombin time international normalized ratioAPPT (activated partial thromboplastin time)Renal function Cardiac enzymes and a 12-lead EKG

Recommended in all patients, but only the assesment of glucose should precede the administration of iv tpa because hypoglycemic may cause focal sings and symptoms that mimic stroke and hyper is associated with unfavorable outcome.platelet count is important on pts taking anticoagulants or liver dysfunction, special consideration to quantitative testing for new anticoagulants may require TT or ecarin clotting time

Regimens for IV rt-PA treatmentInfusion 0.9 mg/ kg (max 90 mg) over 1 hour, 10 % of the dose given as bolus dose over 1 minute Admit to ICU or stroke unitIf severe headache, acute hypertension, nausea, vomiting, or worsening neurological signs, discontinue infusion, and emergency CT brain BP measurement & Neurological assessments every 15 minutesduring & after infusion for 2 hoursevery 30 minutesnext 6 hoursevery houruntil 24 hours

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Regimens for iv rt-PA treatmentDelayed placement of NG tube, bladder catheters, intra- arterial catheters

Anticoagulants and antiplatelet agents should be delayed for 24 hours after treatment

Obtain a follow-up CT or MRI at 24 hours after IV rtPA before starting anticoagulants or antiplatelet agents

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Aspirin (mg)Statins Atorva 40mg 80mgAntacids PPIsAntiepileptics Eptoin (Only if Seizures)AntidepressantsSupportive / Neuroprotectives / Multivitamines 60EUSI ASA RCOP (London)Acute treatment 100-3003253002nd prevention50-32550-300

SECONDARY STROKE PREVENTION:ANTITHROMBOTIC RX BASED ON CAUSE High-flow states:platelets cause clots

Platelets are like Velcrosticking to bumpy wallsLow-flow & hypercoagulable states:clotting factors cause clots

Clotting factors are like dissolved powdered gelatinthat forms clumps of Jello when liquid is staticlarge-arteryatherosclerosissmall-arterydiseasecardioembolismhypercoagulablestate

ANTIPLATELET AGENTaspirin 81-325/dclopidogrel 75/daspirin + dipyridamole XR 25/200 twice/d

ANTICOAGULANTwarfarinINR 2.0-3.0orINR 2.5-3.5

Anticoagulant / HEPARIN

Urgent anticoagulation, with the goal of preventing early recurrent stroke, halting neurological worsening, or improving outcome after acute ischemic stroke, is not recommended (IIIA)

Urgent anticoagulation for management of non-cerebrovascular conditions is not recommended for patients with moderate to severe strokes because increased risk of serious intracranial hemorrhage (IIIA)62ASA Guidelines. Stroke 2013

Anticoagulant

Initiation of anticoagulant therapy within 24 hours of treatment with IV rtPA is not reccommended (IIIB) 63ASA Guidelines. Stroke 2013

AnticoagulantContraindicationsLarge infarctionUncontrollable arterial hypertensionAdvanced microvascular changes in the brain

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SECONDARY STROKE PREVENTION:RISK-FACTOR MODIFICATIONCigarette smoking cessationBupropion Start 150 mg daily x 3 daysThen 150 mg BID x 3 monthsNortriptyline Start 10-25 mg each night gradually to 75 mg each nightNicotine patch/gum/inhalerConcurrent with bupropion or nortriptylineVarenicline Start 0.5 mg daily x 3 days gradually to 1 mg BID x 11 wk

SECONDARY STROKE PREVENTION:RISK-FACTOR MODIFICATIONLifestyleAlcohol:men < 2 oz / d, women < 1 oz / dDiet:Low saturated fat, low Na+, high K+,fruits > vegetables, Mediterranean dietExercise:> 20 min aerobic exercise, > 3 x / wkWeight:maintain BMI 18.5-24.9 kg/m2

Drugs to AvoidEstrogen (oral contraceptives, HRT)Sympathomimetic agents (incl. decongestants, diet pills)NSAIDs (if taking aspirin)PPIs (if taking Plavix)

ISCHEMIC STROKE / TIA2 PREVENTION SUMMARY 2 OF 2Discontinue:Cigarette smokingSympathomimetic agents (incl. decongestants)EstrogensTreat:Carotid stenosis 50/70-99% (CEA or CAS)Sleep apnea (CPAP)Sickle cell disease (monitor TCD, Hgb S < 30%)

ConclusionsAcute stroke is an emergency condition, is the same level as MI, serious traumaEmergency management is needrt-PA & Stroke unit, are the major advancesAppropriate general care are also needTo improve the quality of care :Multidisciplinary/ network approach are very importance

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MRI BRAIN IN HYPERACUTE ISCHEMIC STROKEDWI & ADC: Early infarction visibleFLAIR: No signal changes; possible sulcal effacement in area of infarction

DWIADCFLAIRRRRLLL

INTRACRANIAL MRA:AP VIEWS OF ANTERIOR CIRCULATION

NormalPaucity of R MCA Branchesc/w Embolic Occlusions

RICARICALICALICARMCALMCARACALACA

CAROTID DUPLEXEvaluates carotid arteries in neck (operable area)Excellent screen in the right handsMay not differentiate 99 vs. 100% stenosisNeed contrast angiography for clinically relevant stenosis measurement

Carotid duplex =Doppler (velocities) +B-mode ultrasound(echo picture)

PlaqueCCA

ICA

ECA

ECHOCARDIOGRAPHY:TTE VS. TEELeft VentricleThrombusDilatationSEC/smokeDyskinesisAneurysmIdentifiessource in 37.2% of pts inNSR

SEC/EF 20%LVTRANSTHORACIC ECHOIdentifiessource in30-40% of pts withunknown cause

LAPFOLeft AtriumThrombusDilatationSEC/smokeTumorPFO/IASA > 5 mmEndocarditisAortic ArchAthero > 4 mmThrombusTumorTRANSESOPHAGEAL ECHO

HYPERCOAGULABLE PROFILEPATIENTS < 55 YEARS OLDCBC w/ diff & plateletsPT/aPTTFibrinogenFactor VIIIFactor VIIC-reactive proteinAntithrombin IIIProtein CProtein S (total & free)Lipoprotein (a)Activated protein C resistance (APCR) (& Leiden factor V mutation if APCR -)Prothrombin G20210A mutationAntiphospholipid antibodiesLupus anticoagulantAnticardiolipin absAnti--2-glycoprotein I absAntiphosphatidylserine absMethyltetrahydrofolatereductase (MTHFR) C677T & A1298C mutationsSickle cell screen

Intracranial Hemorrhage

Etiology of ICH TraumaticSpontaneousHypertensiveAmyloid angiopathyAneurysmal ruptureArteriovenous malformation (AVM) ruptureBleeding into tumorCocaine and amphetamine use

Causes of ICH

Hypertensive ICH

Spontaneous rupture of a small artery deep in the brainTypical sitesBasal GangliaCerebellumPonsTypical clinical presentationPatient typically awake and often stressed, then abrupt onset of symptoms with acute decompensation

Ganglionic Bleed

Contralateral hemiparesisHemisensory lossHomonymous hemianopiaConjugate deviation of eyes toward the side of the bleed or downwardAMS (stupor, coma)

Cerebral HemorrhageJPG

Cerebellar Hemorrhage

Vomiting (more common in ICH than SAH or Ischemic CVA)AtaxiaEye deviation toward the opposite side of the bleed Small sluggish pupilsAMS

Cerebellar Hemorrhage

Pontine Hemorrhage

Pin-point but reactive pupilsAbrupt onset of comaDecerebrate posturing or flaccidity Ataxic breathing pattern

Pontine Hemorrhage


Worst headache of my lifePhotophobiaNuchal rigidity SeizuresNausea and vomiting


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Stroke management protocol