Hemiparesis: The Emerging Role of Hemiparesis: The Emerging Role of the Emergency Physician in Stroke the Emergency Physician in Stroke

Management Management

Edward Sloan, MD, MPHEdward Sloan, MD, MPH

Associate ProfessorAssociate ProfessorDepartment of Emergency MedicineDepartment of Emergency Medicine

University of Illinois College of Medicine-ChicagoUniversity of Illinois College of Medicine-ChicagoChicago, ILChicago, IL

Edward Sloan, MD, MPH

ObjectivesObjectives

• Present clinical case history

• Review Emergency Department H&P

• Examine tPA clinical data

• Discuss tPA use in ischemic stroke

• Review other therapies for ischemic stroke

• Answer clinically relevant questions

Edward Sloan, MD, MPH

CaseCase

A 70 year old female developed acute onset of left arm weakness that lasted approximately 15 minutes and then gradually resolved.  She chose to ignore the event and did well until three weeks later she developed complete paralysis of the left arm and pronounced weakness of the left leg; neither resolved and approximately 90 minutes into the event she called EMS.  Past medical history included hypertension and COPD.  Medications: metoprolol, hydrochlorthiazide, and atrovent.

Edward Sloan, MD, MPH

CaseCase On exam, BP 200/120, P 68, RR 18, T 98, and pulse

oximetry showed 94% saturation.  The patient appeared alert though responses were slow.  The patient had bilateral carotid bruits, clear lungs, and a regular rate and rhythm. There was no facial asymmetry, upper extremity motor 5/5 on the right and 0/5 on the left; lower extremity motor 5/5 on the right and 3/5 on the left.  Sensory was intact to light touch and pinprick.  DTRs were 2/2 on the left and 0/2 on the right.  Planter reflex was downgoing on the right and upgoing on the left.

Edward Sloan, MD, MPH

Acute Ischemic Stroke QuestionsAcute Ischemic Stroke Questions

• What are the epidemiology & etiology? • What are the key elements of the exam?• What is the NIH stroke scale?• What did the NINDS trial show?• How should tPA be used by the EM MD?• What about hemorrhagic conversion?• What about other therapies?

Edward Sloan, MD, MPH

Acute Stroke: EpidemiologyAcute Stroke: Epidemiology

• 700,000 Cases annually

• 20% mortality within one year

• $30 billion annual costs

• Ischemic and hemorrhagic strokes

Edward Sloan, MD, MPH

Acute Ischemic Stroke:Acute Ischemic Stroke:EtiologyEtiology

• Thrombotic, embolic, hypoperfusion

• Majority are vessel thrombosis

• Clot formation on diseased vessel

• 20% are embolic, from heart, great vessels

• Hypoperfusion with cardiogenic shock

Edward Sloan, MD, MPH

Acute Ischemic Stroke: SyndromesAcute Ischemic Stroke: Syndromes

• Anterior cerebral• Middle cerebral• Posterior cerebral• Vertebrobasilar• Basilar artery occlusion• Cerebellar • Lacunar• Arterial dissection

Edward Sloan, MD, MPH

Acute Stroke: Historical ElementsAcute Stroke: Historical Elements

• When did symptoms begin? Onset?

• Prior history of similar symptoms?

• When was the patient last seen normal?

• Risk factors?

• Medical hx that would preclude tPA use?

Edward Sloan, MD, MPH

Acute Stroke: Physical ExamAcute Stroke: Physical Exam

• Vital signs, pulse ox, accucheck

• HEENT: Pupils, papilledema, airway

• Neck: Bruits, nuchal rigidity

• Chest: Rales (CHF, aspiration)

• Cardiac: Gallops, murmurs

Edward Sloan, MD, MPH

Acute Stroke: Physical ExamAcute Stroke: Physical Exam

• Abd: Evidence of AAA

• Ext: Evidence of CHF, DVT

• Skin: Evidence of infectious etiology

• Neuro: CN, motor, sensory, reflexes, cerebellar, visual, language,

neglect, mental status

Edward Sloan, MD, MPH

Neurologic Exam: Cranial NervesNeurologic Exam: Cranial Nerves

• CN: Anterior vs. brainstem?– Anterior: Contralateral CN deficits

– Brainstem: Ipsilateral CN deficits

Edward Sloan, MD, MPH

Neurologic Exam: MotorNeurologic Exam: Motor

• Motor: CN, upper & lower ext– CN: Eye motor (Bell’s)

– Upper: Pronator drift

– Lower: Leg lift

Edward Sloan, MD, MPH

Neurologic Exam: SensoryNeurologic Exam: Sensory

• Sensory: Light touch, pinprick

• Graphesthesia

Edward Sloan, MD, MPH

Neurologic Exam: ReflexesNeurologic Exam: Reflexes

• Normal vs. pathologic – Normal: Corneal, gag, DTRs

– Pathologic: Babinski, Chadduck

Edward Sloan, MD, MPH

Neurologic Exam: CerebellarNeurologic Exam: Cerebellar

• Truncal ataxia

• Ataxic gait

• Rhomberg

Edward Sloan, MD, MPH

Neurologic Exam: VisualNeurologic Exam: Visual

• Visual field deficit

• Homonomous hemianopsia– Neglect of one side

Edward Sloan, MD, MPH

Neurologic Exam: LanguageNeurologic Exam: Language

• Dysarthria: Poor speech, motor dysfunction

• Aphasia: Disturbed language processing– Expressive: can’t speak– Receptive: can’t process the spoken word

Edward Sloan, MD, MPH

Neurologic Exam: Mental StatusNeurologic Exam: Mental Status

• Level of consciousness (AVPU)– Alert

– Responds to verbal

– Responds to painful

– Unresponsive

Edward Sloan, MD, MPH

Neurologic Exam: NIH Stroke Neurologic Exam: NIH Stroke ScaleScale

• 13 item scoring system, 7 minute exam • Integrates neurologic exam components• CN, motor, sensory, cerebellar, visual,

language, LOC• Maximum score is 31, signifying severe stroke• Minimum score is 0, a normal exam• Scores greater than 15-20 are more severe

Edward Sloan, MD, MPH

Acute Ischemic Stroke:Acute Ischemic Stroke:NINDS Clinical Trial of tPANINDS Clinical Trial of tPA

• Treatment within 180 minutes

• 0.9 mg/kg of tPA

• Two part study

• Endpoint: favorable outcome at 3 months

• Also examined mortality, hemorrhage

Edward Sloan, MD, MPH

NINDS Clinical Trial of tPA: ResultsNINDS Clinical Trial of tPA: Results

• Good outcome: 30% more patients

• Odds of favorable outcome: 1.7 (1.2-2.6)

• 10x greater hemorrhage risk: (6.4 vs. 0.6%)

• Comparable 3 month mortality: (17 vs. 21%)

• Conclusion: tPA worth the hemorrhage risk, since there is clear benefit

Edward Sloan, MD, MPH

NINDS Clinical Trial of tPA:NINDS Clinical Trial of tPA:Clinical UpshotClinical Upshot

• tPA must be considered

• Patient selection is very difficult

• Must maximize risk/benefit ratio

• Must avoid hemorrhage, if possible

• Need adequate severity, but not too severe

• Less than 2% of patients will meet criteria

Edward Sloan, MD, MPH

NINDS Clinical Trial of tPA:NINDS Clinical Trial of tPA:Timing IssuesTiming Issues

• Early EMS contact is key

• Door to CT and CT read time important

• Is there time for a neurologist to consult?

• A stroke team helps

• The 3 hour window is not the only issue

Edward Sloan, MD, MPH

NINDS Clinical Trial of tPA:NINDS Clinical Trial of tPA:Clinically Relevant IssuesClinically Relevant Issues

• Histories are unreliable

• Timing issues hard to press for stroke

• Patient selection is painfully difficult

• Every CT has a hypodense area

• Tendency not to intervene

• First do no harm

• What we did vs. what was destined to be

Edward Sloan, MD, MPH

tPA in Acute Ischemic Stroke:tPA in Acute Ischemic Stroke:Clinical & Documentation IssuesClinical & Documentation Issues

• Document that tPA was considered• If not used, state explicitly why the pt did

not meet criteria or why it was deferred• When explaining, tell the four key points:

– 30% greater chance of good outcome– 10 fold greater risk of bleeding– Same mortality rate, despite bleeding risk– Explain why mortality is comparable

Edward Sloan, MD, MPH

tPA in Acute Ischemic Stroke:tPA in Acute Ischemic Stroke:Other Relevant StudiesOther Relevant Studies

• ECASS: No efficacy, higher mortality

• IA tPA: Effective, feasible

• ATLANTIS: 5 hour window not possible

• Cleveland: Non-supportive tPA data– 2% treated, 50% standard of care deviation– 16% bled, 3x higher in-hospital mortality

• STARS: Favorable outcome and mortality

Edward Sloan, MD, MPH

Acute Ischemic Stroke: Acute Ischemic Stroke: Goals of Other TherapiesGoals of Other Therapies

• Recanalization

• Stop ischemic cascade

• Minimize hemorrhage

• Minimize morbidity and mortality

Edward Sloan, MD, MPH

Acute Ischemic Stroke:Acute Ischemic Stroke:Other TherapiesOther Therapies

• LMW heparin: Possibly effective• IST study: ASA reduces death & stroke

recurrence by 1% • PROACT II: IA prourokinase improves outcome • STAT: Ancrod (pit viper venom) improves

outcome, but causes hemorrhage• Neuroprotectants: May provide benefit

Edward Sloan, MD, MPH

Acute Ischemic Stroke:Acute Ischemic Stroke:Other IssuesOther Issues

• MR Imaging: Feasible, assists pt selection

• Admission need: Still must admit TIA/CVA pts– No reason not to admit CVAs– Can’t predict progression, complications– Data less clear for TIAs…home observation?– Need HMO experience to be documented

Edward Sloan, MD, MPH

Acute Ischemic Stroke:Acute Ischemic Stroke:Case ManagementCase Management

• Get the CT scan ASAP• Control the blood pressure• Start making calls: PMD, family,

neurologist• Find out the CT results• Decide risk/benefit• Discuss with pertinent decision makers

Edward Sloan, MD, MPH

Acute Ischemic Stroke:Acute Ischemic Stroke:Specific Case OutcomeSpecific Case Outcome

• CT obtained quickly

• BP controlled with time & SL NTG

• NIH stroke scale: 15

• CT showed ?? Low density area

• Neurologist not inclined to treat

• Family defers tPA after consultation

• Some long term deficit, physical therapy

Edward Sloan, MD, MPH

Acute Ischemic Stroke: Acute Ischemic Stroke: ConclusionsConclusions

• Ischemic stroke is a big problem

• There is significant morbidity & mortality

• tPA is effective in a narrowly defined group

• Must aggressively work to get tPA used

• Other therapies hold promise

Edward Sloan, MD, MPH

Acute Ischemic Stroke: Acute Ischemic Stroke: RecommendationsRecommendations

• Better public education

• More timely EMS activation

• More analysis of tPA use re: optimal patients

• Rapid MR imaging

• Dvlp other therapies, esp neuroprotectants

Edward Sloan, MD, MPH

All are true statement about acute All are true statement about acute ischemic stroke except:ischemic stroke except:

a. There are three major categories: thrombotic, embolic, and hypoperfusion.

b. The majority of all strokes are caused by vessel thrombosis.

c. The symptoms of ischemic stroke develop over minutes to hours.

d. The most common source of emboli are the heart and major vessels.

e. Middle cerebral artery infarction is associated with ipsilateral weakness and numbness.