stroke2013update teleron

Update on Acute Ischemic Stroke Management

1/15/2014

Amy Lynn Teleron, MD Assistant Professor, Internal Medicine

UVM College of Medicine PCIM Hospitalist

  Review management of acute ischemic stroke   Discuss updates from the 2013 Stroke Guidelines

by the American Stroke Association (ASA) / American Heart Association( AHA)   Case presentation

  Importance ◦  Availability of neurologists/stroke code teams ◦  Responsibility of primary care physicians/hospitalists ◦  Boards

Jauch, EC et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2013

  65yo female arrives at ED 12:20pm   CC: Vaginal bleeding worsening x 3 days

  HPI: ◦  Never established with physician until last month ◦  Fist-size clots x 2 months ◦  No pelvic exam > 30 years ◦  + fatigue

  New dx of HTN at first PCP visit 1 month prior   Patient wanted to try diet first as treatment ◦  SBP at home 140-150 per patient

  In triage ◦  BP 227/110, Hb 10.2 (baseline 11) ◦  Clonidine 0.2mg PO x 1 given at 15:08

  In ER waiting room ◦  N/V and syncopal episode - given Zofran 15:50

  Patient transferred urgently to ER bed ◦  SBP verbally reported as decreased to 80/40   Given NS 1L bolus 17:00 ◦  New symptoms after syncope & decreased BP included   Right facial droop   Right upper and lower extremity weakness ◦  Examination done by ED physician

  V/S from time of triage ◦  T 36.9, P 98, R 18, BP 227/110, O2 Sat 99%RA, ◦  BMI 28.9

  V/S on M/S exam ◦  T 36, P 61 (NSR), R 15, BP 142/55, O2 Sat 99% RA

  Gen: AAOx3, NAD   Neuro: Droop on right side of mouth only ◦  Slow to respond but appropriate and following commands ◦  CN 2-12 otherwise grossly intact ◦  Neuro exam:   5/5 strength, 2+ DTR throughout, downgoing plantar B/L

  Transfer to step-down unit at 02:00 ◦  Patient is AAO x 3 throughout early am ◦  Completely resolved right sided weakness <1.5 hrs   Initial bedside swallow evaluation failed in ER   Repeated on floor after clinical improvement – passed

  Patient refusing aspirin PR and PO ◦  Neuro checks q2 hours ◦  Pelvic/Transvaginal US for vaginal bleed put on hold

  Transient ischemic attack   Acute stroke ◦  Ischemic ◦  Hemorrhagic

  Clonidine-induced Syncope   Syncope due to acute anemia   Hypertensive emergency   Complicated Migraine   Seizure   Conversion disorder

 What is the definition of TIA?

  Past: Neurological dysfunction up to 24 hours with complete clinical reversal of symptoms.   Arbitrary time threshold too broad   30-50% of classically defined TIA had brain injury on MRI

DWI

  Impossible to define a time cutoff to distinguish if a sx ischemic event will result in brain injury ◦  However, typical duration is <1 or 2 hours

Easton et al. Definition and Evaluation of Transient Ischemic Attack. Stroke, 2009;40:2276-2293.

  ASA/AHA 2009– endorsed revised definition ◦  A transient episode of neurological dysfunction ◦  Caused by focal brain, spinal cord or retinal ischemia ◦  Without acute infarction

◦  Definition is now tissue based, like diagnoses of cancer & MI   Like MI, dx is inferred from clinical, laboratory and

imaging data   Can sometimes be clinical Dx because it may not

be identifiable on imaging ◦  Ie. Small lateral medullary infarcts

Easton et al. Definition and Evaluation of Transient Ischemic Attack. Stroke, 2009;40:2276-2293.

Sacco, RL et al. An updated definition of stroke for the 21st century. Stroke.2013; 44: 2064-2089

  Patients with transient ischemic neurological symptoms should undergo neuro-imaging evaluation within 24 hours of symptom onset or as soon as possible in patients with delayed presentations. MRI, including DWI, is the preferred brain diagnostic imaging modality. If MRI is not available, head CT should be performed   (Class I; Level of Evidence B).   (Unchanged from the 2009 TIA scientific statement6)

Jauch, EC et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2013.

  Noninvasive imaging of the cervical vessels should be performed routinely as part of the evaluation of patients with suspected TIAs ◦  (Class I; Level of Evidence A). ◦  (Unchanged from the 2009 TIA scientific statement)

  Noninvasive imaging by means of CTA or MRA of the intracranial vasculature is recommended to exclude the presence of proximal intracranial stenosis and/or occlusion and should be obtained when knowledge of intracranial steno-occlusive disease will alter management. ◦  (Class I; Level of Evidence A) ◦  (Revised from the 2009 TIA scientific statement6)


 Assuming this was a TIA, what is this patient’s risk of stroke?

  Johnston et al. Lancet 2007 ◦  Scoring system to help physicians make the decision to

admit patient, ie. Treat a TIA as an emergency   In order to optimize stroke prevention

◦  Modified two scoring systems into new unified system   California and ABCD scores   Incorporates elements of both

Feature Points Age >/= 60 years +1 BP >/= 140/90 +1 Clinical Features Unilateral weakness Speech impairment without weakness

+2 +1

Duration >/= 60 minutes 10-59 minutes

+2 +1

Diabetes Mellitus +1

Johnston et al. Lancet 2007

 Risk of stroke at 2 days

◦ Low (0 – 3 points) = 1% ◦ Moderate (4 – 5 points) = 4.1% ◦ High (6 – 7 points) = 8.1%

Feature Points Age >/= 60 years +1 BP >/= 140/90 +1 Clinical Features Unilateral weakness Speech impairment without weakness

+2 +1

Duration >/= 60 minutes 10-59 minutes

+2 +1

Diabetes Mellitus +1

Johnston et al. Lancet 2007

 Risk of stroke at 2 days

◦ Low (0 – 3 points) = 1% ◦ Moderate (4 – 5 points) = 4.1% ◦ High (6 – 7 points) = 8.1%

  At 10:00 patient given labetalol 10mg IV for BP 215/98   Order written PRN for SBP > 190

  At 12:30, M/S resident called d/t patient confusion & R-sided weakness ◦  BP documented as 106/53 at that time, Patient in Afib rate 80’s ◦  Labetalol order d/c’d ◦  Patient refusing more medications ◦  Neuro exam documented but no NIHSS documented

  SBP rises to 180-190’s and remains stable

  Stat CT head without contrast ordered

  Should you give rtPA to the patient?

  How do you manage the blood pressure in acute stroke?

  Should you start a heparin gtt for new atrial fibrillation?

 Should this patient receive IV rtPA??

rtPA = recombinant tissue plasminogen activator

  Frank hypodensity on NECT may increase the risk of hemorrhage with fibrinolysis and should be considered in treatment decisions.

  If frank hypodensity involves more than one third of the MCA territory, intravenous rtPA treatment should be withheld ◦  (Class III; Level of Evidence A). ◦  (Revised from the 2009 imaging scientific statement 9)


  This patient had witnessed onset of: ◦  Right facial droop ◦  Right sided weakness ◦  (Within the window for administration)

  However: ◦  Hypodensity on CT head involved more than one third of

the MCA territory ◦  Uncontrolled BP (patient refusing meds)

  Therefore, patient NOT a candidate for rtPA

  Recommendations to lower BP in candidates for acute reperfusion therapy (Updated AHA/ASA 2013)

  If SBP >185 or DBP >110 ◦  Labetalol 10 to 20 mg IV over 1 to 2 minutes   May repeat x 1 ◦  OR Nicardipine infusion, 5 mg/h, titrate up by 2.5 mg/h at 5- to

15-minute intervals, maximum dose 15 mg/h; when desired blood pressure attained, adjust to maintain BP goals ◦  Other agents (hydralazine, enalaprilat, etc) may be considered

  If BP is not maintained at or below 185/110 mm Hg, do not administer rtPA


  If medications are given to lower blood pressure, the clinician should be sure that the blood pressure is stabilized at the lower level before treating with IV rtPA and maintained below 180/105 mm Hg for at least the first 24 hours after IV rtPA treatment.


  Maintain BP at or below 180/105 mm Hg: ◦  Monitor BP q15 minutes x 2 hrs from the start of rtPA

therapy, then q30 minutes x 6 hrs, then q1 hr x 16 hrs   If systolic BP >180–230 mm Hg or diastolic BP

>105–120 mm Hg: ◦  Labetalol 10 mg IV followed by continuous IV infusion 2–

8 mg/min; or ◦  Nicardipine 5 mg/h IV, titrate up to desired effect by 2.5

mg/h every 5–15 minutes, maximum 15 mg/h   If BP not controlled or diastolic BP >140 mm Hg,

consider IV sodium nitroprusside Jauch, EC et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke. Stroke 2013.

  Symptomatic Intracerebral Bleeding   Systemic bleeding   Myocardial rupture if fibrinolytics are given within a

few days of acute myocardial infarction,   Reactions such as anaphylaxis or angioedema

(1.3-5.1%)

  If hypotension present, correct to limit further cellular damage ◦  Hypotension = Blood pressure that is lower during acute

ischemic stroke than the premorbid pressure

  Appropriate tx in acute stroke is still CONTROVERSIAL ◦  Ongoing study: CHHIPS in J Hypertens

  Controlling Hypertension and Hypotension Immediately Post-Stroke


  AHA/ASA Guidelines 2013 ◦  “Reasonable goal”   Lower BP by 15% on the first day (Class I)

  (changed from 15-25% from 2007 Guidelines) ◦  Consensus is to treat only if SBP >220 or DBP >120


  Data inconclusive and conflicting ◦  An ideal blood pressure range has not yet been

scientifically determined.

  Initiating antihypertensive therapy within 24 hours is relatively safe

  Reasonable to restart BP meds after 24 hours   Both Class IIa indications (new in 2013)


  Schrader et al. in Stroke 2003 (noted in 2007 ASA/AHA Guidelines) ◦  Day 2: Medications increased if SBP > 160 or DBP > 100 ◦  Day 7: Added antihypertensives if persistent high BP’s

  For every 10mmHg increase > SBP 180, ◦  Risk of neuro deterioration increases by 40% ◦  Risk of poor outcome increases by 23%

  Should you start a heparin gtt on this patient since she now has new Afib (rate of 80’s) in the setting of acute stroke?

  What about stroke in Atrial Fibrillation?

  Urgent anticoagulation, with the goal of preventing early recurrent stroke, halting neurological worsening, or improving outcomes after acute ischemic stroke, is not recommended for treatment of patients with acute ischemic stroke

  (Class III; Level of Evidence A).   (Unchanged from the previous guideline13)


 So what happened to the patient?

  Absence of normal flow to a large part of the L frontal and frontoparietal lobe and left temporal lobe due to what appears to be an occlusion of the L-ICA

  There is very little cross filling from an ACOM   The Left Anterior communicating artery does not

appear to provide cross filling from the left A2 segment but I do not see strong A1 segment or enough A1 segment to replace the left MCA.

  Basilar system in tact.

  65 yo WF presented with vaginal bleeding and hypertensive urgency SBP 220’s ◦  Likely acute carotid occlusion causing increased BP

  BP acutely dropped TIA ◦  Syncope and R-sided facial droop & weakness

  Symptoms resolved within 2 hours   BP decreased in hospital Acute ischemic stroke ◦  Combined L-ICA occlusion & incomplete Circle of Willis

  The usefulness of emergent or urgent CEA when clinical indicators or brain imaging suggests a small infarct core with large territory at risk (eg, penumbra), compromised by inadequate flow from a criti- cal carotid stenosis or occlusion, or in the case of acute neurological deficit after CEA, in which acute thrombosis of the surgical site is suspected, is not well established

  (Class IIb; Level of Evidence B).   (New recommendation)

  In patients with unstable neurological status (either stroke-in-evolution or crescendo TIA), the efficacy of emergent or urgent CEA is not well established

  (Class IIb; Level of Evidence B).   (New recommendation)


  BP control within 24 hours of acute ischemic stroke ◦  Decrease BP 15% only ◦  PRN BP med only if SBP >220 or DBP > 120

  NIH Stroke Scale (NIHSS) ◦  Ensures that the major components of a neurological

examination are performed in a timely and uniform fashion. ◦  Helps select patients for various interventions ◦  Facilitates communication

  Other admission orders ◦  Aspirin (initial dose 325mg) within 24 – 48 hours   Not recommended within 24 hours of IV fibrinolysis   Data do not provide solid evidence about the utility of other

antiplatelet agents (ASA/AHA 2013 Stroke Guidelines)   ? Dipyramidole + aspirin superior to aspirin alone (Lancet 2006)   ? Plavix (NEJM 2008)

  New studies with antiplatelets cont to be underway ◦  Telemetry for minimum 24 hours (Class I) ◦  Keep 02 Sats >94% (Class I) ◦  Goal blood glucose 140-180 (Class IIa)

  What about stroke in Atrial Fibrillation?

  Urgent anticoagulation, with the goal of preventing early recurrent stroke, halting neurological worsening, or improving outcomes after acute ischemic stroke, is not recommended for treatment of patients with acute ischemic stroke

  (Class III; Level of Evidence A).   (Unchanged from the previous guideline13)


  Highlights on IV rtPA administration ◦  Window: 3 to 4.5 hours ◦  Recall indications/contraindications (see tables prior)

  Intra-arterial rtPA administration ◦  Can be given in major ischemic strokes <6 hours caused

by occlusions of MCA

◦  tPA considered* ◦  Screen for dysphagia ◦  Deep vein thrombosis prophylaxis* ◦  Lipid profile within 48 hrs of hospitalization ◦  Smoking cessation ◦  Education about stroke* ◦  Plan for rehabilitation considered* ◦  Antithrombotic medications started within 48 hours* ◦  Antithrombotic medications prescribed at discharge* ◦  Anticoagulants prescribed to patients with A fib* ◦  Discharged on statin medication* ◦  (Or documentation why meds not prescribed)

*Those included in “Stroke Core Measure Set” http://www.jointcommission.org/assets/1/6/Stroke.pdf

  Large vessel occlusion accounted for 46% of acute stroke

  Presence of large vessel occlusion was associated with a 4.5-fold increased odds of death

  Angiographic status of vessels is informative at the time of hospital presentation. ◦  Wide variation in NIHSS scale scores despite identical

vascular segment occlusion ◦  May improve decision-making , ie. endovascular

intervention

Smith et al. Stroke and TIA Significance of Large Vessel Intracranial Occlusion Causing Acute Ischemic. Stroke 2009. STOP Stroke Study

  Future possibilities – studies underway ◦  Emergent CEA   Various studies: 21-42% mortality ◦  Emergent endovascular interventions ◦  Urgent open embolectomy for cardioembolic occlusion   Ie. in patients with atrial fibrillation