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    Management of Acute Ischemic
               Stroke Patients



                   Jiann-Shing Jeng, MD, PhD
            Stroke Center & Department of Neurology
       National Taiwan University Hospital, Taipei, Taiwan
Stroke Types:   NTUH, 1995~2007
2

                      Large artery
                     atherosclerosis
                          12%             Small artery lacune
    Subarachnoid                                 22%
     hemorrhage
        6%

                                                    Cardioembolism
                                                         14%



         Cerebral
        hemorrhage                        Other determined
           22%             Undetermined          4%
                               20%
Stroke Chain of Survival
3
       Detection Recognition of stroke signs/symptoms
       Dispatch Call 119 and priority EMS dispatch
       Delivery Prompt transport and prehospital notification to hospital
       Door         Immediate ED triage
       Data        ED evaluation, prompt laboratory studies, and CT imaging
       Decision Diagnosis and decision about appropriate therapy
       Drug        Administration of appropriate drugs or other intervention
EMS in Acute Stroke
4
       Rapid identification of acute stroke
       Elimination of comorbid conditions mimicking stroke
       Stabilization
       Rapid transportation
       Notification of receiving institution
Prehospital Stroke Identification
5


       Los Angeles Prehospital Stroke Screening


       Cincinnati Prehospital Stroke Scale
Los Angeles Prehospital Stroke Screen
    (LAPSS)
6
        Last time patient known to be symptom free
        Screening criteria
          1.   Age >45 y
          2.   No history of seizure or epilepsy
          3.   Symptom duration less than 12 hours
          4.   No previously bedridden or wheelchair bound
          5.   Blood glucose 60-400 mg/Dl
          6.   Exam:
                  Facial smile/grimace: normal, droop
                  Grip: normal, weak grip, no grip
                  Arm strength: normal, drifts down, falls rapidly
LOS ANGELES MOTOR SCALE
    (LAMS)
7
                    Normal          Right                  Left          Total

    Facial                   Ͱ Droop (1)           Ͱ Droop (1)
                    Ͱ (0)
    smile/grimace

                             Ͱ Weak grip (1)       Ͱ Weak grip (1)
    Grip            Ͱ (0)
                             Ͱ No grip (2)         Ͱ No grip (2)

                    Ͱ (0)    Ͱ Drifts down (1)     Ͱ Drifts down (1)
    Arm strength
                             Ͱ Falls rapidly (2)   Ͱ Falls rapidly (2)

                                                        TOTAL Score
Cincinnati Prehospital Stroke Scale
8
       Facial droop
           Normal : both sides of face more equally
           Abnormal : one side of face does not move as well as the
            other
       Arm drift
           Normal : both arms move the same or both arms do not move
            at all
           Abnormal : one arm either does not move or drift down
            compared to the other
       Speech
           Normal : says correct words with no slurring
           Abnormal : slurs words, says the wrong words, or is unable to
            speak
How to approach a patient with
    probable acute stroke?
9
       New onset of acute                        Subsequent hospital
        neurological deficit                       management
            Differential diagnosis of other           Acute stroke
             non-stroke diseases
                                                        management
                                                       Establish cause of
       Initial ER assessment and                       stroke
        management                                     Stroke risk factors
            Vital signs, sugar                        Dysphagia screening
            Consciousness: GCS                        Early rehabilitation
            Non-contrast head CT                         PT,   OT, ST
            Stroke severity: NIHSS                    Plan for secondary
            Stroke type and location                   prevention of stroke
            Hyperacute management
               Thrombolytic therapy
               Craniectomy

               Intensive care/monitoring
History for initial diagnosis of acute stroke
10
        Rapid, accurate history taking
            Often from the family members

        Key elements of history
            Onset time: the last time of normal neurological status
            Onset mode: sudden, acute, subacute
            Onset symptoms: focal or generalized symptoms
            Course: progression of symptoms
            Co-morbid diseases: HTN, DM, Heart diseases, etc.
            Use of medications: antiplatelets, anticoagulants,
             antihypertensives, insulin, etc.
Misdiagnosis of Acute Stroke
      ~ NTUH experience
11

                                          No.      %
     Acute stroke                         2226    87.6


     Misdiagnosis of acute stroke          316    12.4
       Possible neurovascular disorders     57           2.2
       Other neurological disorders        209     8.2
       Non-neurological disorders           50     2.0
     Total                                2542   100.0
Differential Diagnosis of Acute Stroke
12
        Old cerebrovascular disease
        Craniocerebral/cervical trauma
        Meningitis/encephalitis
        Hypertensive encephalopathy
        Intracranial mass (tumor, subdural/epidural hematoma)
        Seizure with persistent neurological signs (Todd’s paralysis)
        Vestibulopathy
        Spinal cord or peripheral nerve lesions
        Migraine with persistent neurological signs
        Metabolic:
             Hyperglycemia
             Hypoglycemia
             post-cardiac arrest hypoxia
             Infection
             Drug overdose, etc.
NTUH ER Stroke Assessment:
     History
13
     Stroke/TIA Onset Time: 確定          年     月     日    時     分 不確定
     Stroke/TIA Onset Symptoms:
        drowsiness, stupor, delirium, coma, headache, vomiting, neck stiffness,
        seizures, anopia, aphasia ( sensory, motor), apraxia, vertigo,
        dizziness, dysarthria, dysphagia, diplopia, ataxia, incontinence
        left side weakness ( face, upper limb, lower limb),
        right side weakness ( face, upper limb, lower limb),
        left side numbness ( face, upper limb, lower limb),
        right side numbness ( face, upper limb, lower limb),
      Others:
     Stroke/TIA Onset Mode: sudden, acute, fluctuating course
     Activity at Stroke/TIA Onset: strenuous activity, ordinary activity, rest, sleep

     Stroke in Progression: yes (symptoms progression>1 hour), no
NTUH ER Stroke Assessment: NIHSS
14
 1a. Level of Consciousness (LOC)       4. Facial Palsy                    7. Limb Ataxia
 □ 0= Alert                             □ 0= Normal                        □ 0= Absent
 □ 1= Not alert, but arousable          □ 1= Minor                         □ 1= Present in one limb.
 □ 2= Not alert, obtunded               □ 2= Partial                       □ 2= Present in two limbs
 □ 3= Uunresponsive                     □ 3= Complete                      8. Sensory
 1b. LOC Questions                      5a Left Motor Arm                  □ 0= Normal
 □ 0= Answers both questions            □ 0= No drift                      □ 1= Mild to moderate sensory loss
      correctly                         □ 1= Drift                         □ 2= Severe
                                        □ 2= Some effort against gravity
 □ 1= Answers one question correctly                                       9. Best Language
                                        □ 3= No effort against gravity
 □ 2= Answers neither question          □ 4= No movement                   □ 0= normal
      correctly                         5b. Right Motor Arm                □ 1= Mild to moderate aphasia
 1c. LOC Commands                       □ 0= No drift                      □ 2= Severe aphasia
 □ 0= Performs both tasks correctly     □ 1= Drift                         □ 3= Mute, global aphasia
 □ 1= Performs one task correctly       □ 2= Some effort against gravity   10. Dysarthria
 □ 2= Performs neither task correctly   □ 3= No effort against gravity     □ 0= Normal
 2. Best Gaze                           □ 4= No movement                   □ 1= Mild to moderate
 □ 0= Normal                            6a. Left Motor Leg                 □ 2= Severe
 □ 1= Partial gaze palsy                □ 0= No drift                      11. Extinction and Inattention
 □ 2= Forced deviation or total gaze    □ 1= Drift                         □ 0= Normal
      paresis                           □ 2= Some effort against gravity   □ 1= One sensory modality
 3. Visual                              □ 3= No effort against gravity     □ 2= More than one sensory modality
 □ 0= No visual loss                    □ 4= No movement
 □ 1= Partial hemianopia.               6b. Right Motor Leg
 □ 2= Complete hemianopia               □ 0= No drift                      Total Score:
 □ 3= Bilateral hemianopia              □ 1= Drift
                                        □ 2= Some effort against gravity
                                        □ 3= No effort against gravity
                                        □ 4= No movement
NTUH ER Stroke Assessment:
                  Diagnosis
15
     Head CT Findings:
      □Hemorrhage
      □Ischemia
        Early sign:

     Diagnosis:
     □Ischemic Stroke (□ left, □right )
      □ACA; □MCA, total; □MCA, partial; □PCA; □Brainstem, □cerebellum
     □Hemorrhagic Stroke (site:              )
     □Others:

     Management Suggestion:
Head images for acute stroke
     diagnosis
16
     Everyone with suspected stroke
        CT without contrast


     Some patients required stroke mechanism realization
       or treatment consideration
        MRI
        MRA
        CTA
        Ultrasound (duplex, transcranial Doppler, Echocardiography)
        Conventional angiography
Early CT signs in acute MCA stroke
17




 Left and middle: Hyperdense left MCA sign (yellow arrow), hypoattenuated left basal
 ganglia (red arrow), and cortical swelling (blue arrows) in the same patient. Right:
 Dot sign (yellow arrow) in the left sylvian fissure.
Alberta Stroke Program Early CT Score (ASPECTS)
  Quantify the extent of CT hypodensity in acute
                      stroke




                            A
                   M1
                            C
                    I
                        L
              M2
                        IC


               M3

                            P




                                Barber et al. Lancet. 2000;355:1670-4.
Diagnosis of Acute Stroke
19
        Stroke vs. non-stroke
        Infarction or hemorrhage
        Infarction
            Location diagnosis
            Arterial territory diagnosis
            Pathophysiology diagnosis
            Etiology diagnosis
Location Diagnosis of Stroke
20
        Supratentorial site
            Hemisphere side
            Cortical or subcortical areas
            Frontal, parietal, temporal lobe

        Infratentorial site
            Midbrain, pons, medulla, cerebellum
Arterial Territory Diagnosis of Stroke
21
        ICA: more than MCA territory
        ACA
        MCA
            Lenticulostriate artery
            Cortical branches
            Internal borderzone area
        PCA
        External borderzone area
        V-B system
            Extracranial VA
            Intracranial
                VA, BA, PICA, AICA, SCA
Acute Stroke Case
22

        A 70-year-old, right-handed man has been known to
     have previous history of poorly controlled hypertension,
     diabetes, and cardiac arrhythmia. He developed abrupt
     onset of left-sided weakness after dinner at 7 pm.



                           What should you do?
Acute Stroke Case
23
         He brought to a medical center ER by the EMS at
     8:30 pm.
         On initial ER arrival, his consciousness was awake,
     blood pressure was 210/120 mmHg, pulse rate was
     120/min irregularly, respiratory rate was 20/min, body
     temperature was 37°C and blood sugar was 320 mg/dL.


                 What should you do if you are on duty at ER ?
Acute Stroke Case
24
           Neurologically, he had flaccid hemiplegia and right-
     sided gaze preference with dense left-sided hemineglect.
     The NIHSS score was 17. Head CT scan revealed
     effacement of cortical sulcal marking in the right middle
     cerebral artery territory and hyperdense MCA sign.



                  What is your diagnosis of the stroke ?
                  What are the next you will do ?
Diagnosis of Acute Stroke
25
        Stroke  confirmed by history and
         images
        Infarction  confirmed by head CT
        Location  right MCA territory (>1/2)
        Arterial territory  right MCA, main trunk
        Pathophysiology  embolism
        Etiology  cardioembolism, atrial
Arterial      Occlusion
Embolism          Site




            Microembolus


              Atheroma
Stroke Evaluation Targets for Potential
     Thrombolytic Candidates
27
                                         Time Target

     Door to doctor                      10 minutes
     Door to CT completion               25 minutes

     Door to CT read                     45 minutes

     Door to treatment                   60 minutes

     Assess to neurological expertise    15 minutes

     Assess to neurosurgical expertise     2 hours

     Admit to monitored bed                3 hours
Acute Ischemic Stroke Protocol
28
                                            ER arrival

                            Triage nurse confirm stroke onset time < 4 hours


     ER Resident performs
     Rapid evaluation (5 minutes)                      Neurology Resident receives
     1.exact time of onset                             ER stroke page and
     2.important history                               proceeds to ER
     3.quick neurological evaluation                   brief history & physical exam
     STAT CT and blood work                            Page Stroke VS

             Head CT findings, laboratory data, NIH stroke scale
             Confirm the criteria fulfilling thrombolytic therapy for ischemic stroke
             Family’s agreement for thrombolytic therapy

           Stroke onset < 3 hours        Stroke onset 3-6 hours          Call Neuroradiologists
           IV-tPA treatment              IA thrombolytic therapy         IA thrombolysis


                  Patient is admitted to Stroke ICU for intensive monitoring/care
Essentials of Acute Stroke Care
29
        Acute stroke team
            Multi-disciplinary care
        Stroke units
        Intensive care of stroke patients
        Standardized protocol of acute stroke management
        Early rehabilitation of acute stroke patients
Acute Stroke Teams
30
        Acute stroke team consists of health care
         professional with experience and expertise in
         stroke
        Available 24 hours everyday, within 15
         minutes of the call
        At a minimum, a qualified acute stroke
         physician and another health care
         professional
Stroke Units
31
        A setting designed for the care of
         stroke
            Admission/discharge criteria, patient census
             and outcome data
            Staffed and directed by personnel (physicians,
             nurses, etc.) with training and expertise in
             caring for patients with cerebrovascular
             disease
            Equipment and written protocols for stroke
             patient care: Neuro, Cardiac, B/P monitoring
Potential Benefits of Stroke Units
32

                                         50
 Cases saved from death and dependency




                                         45
                                         40
                                         35
            per 1,000 events




                                         30
                                         25
                                         20
                                         15
                                         10
                                          5
                                          0
                                              Stroke unit   ASA   tPA <3h         tPA <6h       Neuroprotective
                                                                                                    agents

                                                                   Gilligan et al. Cerebrovasc Dis. 2005;20:239-44.
Goal of Acute Ischemic Stroke Care
33
     Treatment goals                                      Therapeutic strategies

     To reverse brain ischemia before it cause            Recanalization, esp.
      permanent brain injury                              thrombolysis

     To prevent stroke in evolution and recurrence        Antithrombotic agents

     To optimize the patient’s medical condition and      Homeostasis of the brain
      prevent the common medical sequelae that
      occur after stroke or after a stroke intervention

     To optimize functional recovery after the            Early rehabilitation
      residual permanent injury that has occurred
Homeostasis of the Brain
34

      Blood   pressure  SBP 120-220 mmHg, DBP 70-
      110 mmHg
      Blood   glucose level  blood sugar 100-150 mg/dL
      Body   temperature  <37.5°C
      Oxygen   saturation  >95%
Blood Pre s s ure in Ac ute Is c he mic
     S troke
35

         A spontaneous increase in BP is common in
          patients with acute ischemic stroke, and the
          increase in BP tends to be more pronounced in
          patients with preexisting hypertension.

         Elevations in systolic blood pressure >160 mm Hg
          are detected in 60% of patients with acute stroke.
C aus e of Ele vate d Blood Pre s s ure in
     Ac ute S troke
36
        Stress of hospitalization
        Stress of the cerebrovascular event
        A full bladder, nausea, pain, other body
         discomfort
        Preexisting hypertension
        A physiological response to hypoxia
        A response to increased intracranial pressure
Blood Pre s s ure in Ac ute Is c he mic
                        S troke
37
        In a majority of patients, BP tends to decline in the
         first few days to weeks after stroke onset, even
         without pharmacological intervention.

        A significant decline in BP can be seen in
         approximately a third of patients in the first few
         hours after stroke onset.
Blood Pre s s ure in Ac ute Is c he mic
                        S troke
38

        BP often falls spontaneously when the patient is
         moved to a quiet room, the patient is allowed to rest,
         the bladder is emptied, or the pain is controlled.

        In addition, treatment of increased intracranial
         pressure may result in a decline in BP.
Time course of blood pressure (MAP) with
              acute ischemic stroke
39




                       Christensen et al. Acta Neurol Scand 2002;106:142-7.
Admission Blood Pressure and Outcome
     ~ International Stroke Trial
40




                                    Leonardi-Bee et al. Stroke 2002;33:1315-20.
High Blood Pressure in Acute Stroke and
     Outcome
41

        For every 10-mm Hg increase >180 mm Hg, the risk
         of neurological deterioration increased by 40% and
         the risk of poor outcome increased by 23%
Cerebral Perfusion Pressure
42
        Cerebral perfusion pressure (CPP) = Mean
         arterial blood pressure (MABP) – intracranial
         pressure (ICP)
        Maintain CPP >60 mm Hg to ensure
         cerebral blood flow
        In case of elevated ICP, elevated BP is
         required for maintaining adequate CPP.
Management of Elevated BP in Acute
     Ischemic Stroke
43
        Current recommendation based on the type of stroke
        Antihypertensive therapy in acute ischemic stroke
          Aggressive  antihypertensive therapy may lower the cerebral
           perfusion pressure and lead to stroke worsening
          Acute stroke patient may have exaggeration of response to
           antihypertensive agents
          For   nonthrombolytic candidates
           Not to treat if SBP <220, DBP <120, or MAP <130
             mm Hg.
          For   thrombolyic candidates
           Not     to treat if SBP <185, or DBP <110 mm Hg
BP Lowe ring in Ac ute Is c he mic
                     s troke
44

        When treatment is indicated, lowering the BP
         should be done cautiously.

        Some strokes may be secondary to
         hemodynamic factors, and a declining BP may
         lead to neurological worsening.
Blood Pressure Management of Ischemic
     Stroke (nonthrombolytic candidates)
45
     Blood pressure           Treatment

     DBP >140 mm Hg           Sodium nitroprusside (0.5 ug/kg/min).
                              Aim for 10-20% reduction in DBP.
     SBP >220, DBP >120, or   10-20 mg labetalol IV push over 1-2 min.
     MAP >130 mm Hg           May repeat or double labetalol every 20 min
                              to a maximum dose of 150 mg.

     SBP <220, DBP <120, or   Emergent antihypertensive therapy is
     MAP <130 mm Hg           deferred in the absence of aortic dissection,
                              acute myocardial infarction, severe
                              congestive heart failure, or hypertensive
                              encephalopathy
Intravenous Medications Considered for Control
      of Elevated BP in Patients With ICH ~ AHA, 2007
46
     Drug                     Bolus Dose               Continuous Infusion Rate

     Labetalol           5~20 mg every 15 min         2 mg/min (maximum 300 mg/d)

     Nicardipine                  NA                           5~15 mg/h

     Esmolol         250 μg/kg IV push loading dose        25~300 μg/kg/min

     Enalapril       1.25~5 mg IV push every 6 h*                   NA

     Hydralazine     5~20 mg IV push every 30 min           1.5~5 μg/kg/min

     Nipride                      NA                       0.1~10 μg/kg/min

     Nitroglycerin                NA                         20~400 μg/min

                                                            Broderick et al. Stroke. 2007;38.
Common Intravenous Anti-
     Hypertensive Drugs Use in ICU
47

        Sodium Nitroprusside (Nipride)
            Direct vasodilation

        Labetalol (Trandate)
            β and α-1 blockade

        Nicardipine (Perdipine)
            Calcium channel blockade
Sodium Nitroprusside
48
     Mechanism : Direct artery and vein dilation
     Administration : IV infusion
     Onset : Seconds
     Duration : Continuous, during infusion
     Advantage : Balanced ↓ of preload & afterload
     Disadvantage : 1. Excessive hypotension
                      2. Reflex tachycardia
                      3. Light sensitivity
                      4. Potential cyanide/thiocyanate toxicity
     Dosage : 0.25-10 µg/kg/min IV
Labetalol
49
     Mechanism : β and α-1 blockade
     Administration : Bolus/infusion
     Onset : bolus -- 5~30 min, infusion -- 15~60 min
     Duration : 2~12 hrs
     Advantage : 1. Little change in HR and CO
                  2. Intra-A or ICU monitoring (-)
     Disadvantage : 1. Orthostatic hypotension
                       2. Urinary retention
                       3. β-blocker’s contra-indications
     Dosage : 10-80 mg IV q10 min up to 300 mg,
              IV infusion: 0.5-2 mg/min
Nicardipine
50
     Mechanism : Calcium blockade, endothelin-1 antagonism
     Administration : Bolus/infusion
     Onset : 1-5 min
     Duration : 3~6 hrs
     Advantage : 1. no interference with CBF, CO
                   2. diuretic effect
                  3. inhibit platelet aggregation, vasospasm
     Disadvantage : 1. hypotension
                       2. bradycardia
     Dosage : 5 mg/h IV, 2.5 mg/h q15 min, up to 15 mg/h
Blood Glucose within the first 48
     hours after stroke
51
        124 patients with ischemic stroke without previously
         diagnosed diabetes had blood glucose measured at
         least 4-hourly until 48 hours poststroke.

        The mean glucose was 6.6 mmol/L throughout the
         period of monitoring, with no change over time.

        More severe stroke and glucose-lowering therapy to be
         associated with higher poststroke glucose levels.

                                            Wong et al. Neurology 2008;70:1036-41.
Poststroke Hyperglycemia
52
        Persistent hyperglycemia
            Definition: mean blood glucose >7 mmol/L (126
             mg/dL) or HbA1C >6.2%
            An independent determinant of infarct expansion
            Associated with worse functional outcome




                                           Baird al. Stroke. 2003;34:2208-14.
Intensive Insulin Therapy in the Medical ICU
53
        A prospective, randomized, controlled study of 1,200
         adult patients admitted to the medical ICU.
        Comparison between conventional therapy (insulin
         administered when blood glucose >215 mg/dL) and
         intensive therapy (blood glucose control within 80-110
         mg/dL)
        Intensive insulin therapy significantly reduced morbidity
         among all patients in the medical ICU.

                                  Van den Berghe et al. N Engl J Med. 2006;354:449-61.
Respiratory Failure in Acute Stroke
     Patients
54
        Major causes                   Prognosis: poor in
            Aspiration pneumonia        49-93%
            Impaired central
             respiratory drive          Respiratory function
            Neurogenic pulmonary
                                          Risk for aspiration,
             edema
                                           airway obstruction,
        Overall stroke: 10%
                                           hypoventilation.
            Ischemic stroke: 5-6%        Target at O2
            ICH: 26-30%
                                             saturation > 95%
            SAH: 47%
Fever and ischemic stroke
55
        Fever correlates with increased severity of stroke,
         mortality, and poorer prognosis in patients with ischemic
         stroke
        Differentiation of the fever causes
            central, drug, infection, etc.
        Hyperthermia
            May accelerate cerebral metabolism and neuronal injury
            A marker of severity of stroke or a consequence of large
             strokes is unclear
        Mild hypothermia
            Improve neurological outcome
            Reduce elevated ICP
Causes of Intracranial Hypertension
56
        Intracranial mass
        Cerebral edema
            Cytotoxic (intracellular)
            Vasogenic (extracellular)
        Cerebrospinal fluid hypervolemia
            Decreased absorption
            Overproduction of CSF
        Increased intracranial blood volume
            Cerebral vasodilatation (hypoxia, hypercapnia)
            Obstructed venous outflow
IICP Management in Acute Ischemic Stroke
57
     General                              Osmotherapy
        cardiopulmonary and                   Mannitol
        metabolic support                      Glycerol
        Positioning:elevate head of
                                               Hypertonic saline
        the bed to 30o                     Hyperventilation
        Treat   fever
                                           Surgery
        Treat   seizure                       Drainage of
        Avoidhypoxia and                       cerebrospinal fluid:
        hypercapnia                             ventriculostomy, VP
                                                shunt
        Avoid    hypo-osmolar fluids          Craniectomy
        Avoid    hyperglycemia
Medical Therapy in Acute Ischemic
     Stroke
58
        Thrombolytic therapy
            IV rt-PA therapy
            IA rt-PA or urokinase therapy
            Combined IV and IA thrombolysis
        Antithrombotic therapy
            Antiplatelets: aspirin, clopidogrel (Plavix), Aggrenox
            Anticoagulants: heparin, low-molecular weight heparin,
             warfarin
        Neuroprotection: uncertain effect
Territory infarct vs. borderzone
     infarct
59
Penumbrae of Ischemic Stroke
60
                          Penumbrae is the target
                           of any reperfusion
                           therapy
                          The fate of brain tissue
                           depends on
                              Time
                              Cerebral blood flow
                                   Occluded arterial flow
                                   Collateral blood flow

                          Time is brain
Outcomes in rt-PA-treated Patients Compared with
               Controls at 3 M After Stroke
61




                                       NINDS rt-PA Study Group. NEJM 1995;333:
IV Thrombolysis of Acute Ischemic
     Stroke
     ~ Cochrane Meta-Analysis
62
 death or dependency (mRS 3-6)    death or dependency (mRS 3-6)
 treated up to 3 h after stroke   treated up to 6 h after stroke
Model Etimating OR for Favourable Outcome at 3
     M in rt-PA-treated Patients Compared with
     Controls
63




                                          Hacke et al. Lancet 2004;363:768-774
Cochrane thrombolysis meta-analysis
     symptomatic (including fatal) intracranial hemorrhage
64
 Outcome in SITS-MOST and Pooled Randomised
  Controlled Trials at 3 M After Stroke Onset
65




      Wahlgren et al. Lancet 2007;369:275-82.
ECASS III : IV rt-PA 3~4.5 hours
         Distribution of Scores on the Modified Rankin Scale
66




Hacke et al. N Engl J Med. 2008;359:1317-29.
ECASS III : IV rt-PA 3~4.5 hours
     Odds Ratios for Functional End Points at Days 90 and 30 after
     Treatment
67




                                             Hacke et al. N Engl J Med. 2008;359:1317-29.
IV tPA for Acute Ischemic Stroke
     ~ Inclusion Criteria
68
        Ischemic stroke with clearly defined symptom onset
        Measurable deficit on the NIH Stroke Scale
        Age >18 years
        No evidence of intracranial blood on the brain CT scan
        Timing from the symptom onset to initiate of IV rt-PA
            NINDS (1995) : <3 hours
            ECASS-III (2008) : <4.5 hours
IV tPA for Acute Ischemic Stroke
     ~Exclusion Criteria
69
        Rapidly improving or minor stroke symptoms (NIHSS <4)
        Severe stroke symptoms by clinical (e.g., NIHSS >25) or head
         CT scan (> 1/3 MCA low density)
        Stroke or serious head trauma within 3 mo
        Major surgery within 14 d
        History of intracranial hemorrhage
        Systolic BP >185 mmHg or diastolic BP >110 mmHg of
         treatment initiation
        Aggressive BP treatment (i.e., continuous IV infusion of
         antihypertensive to achieve above goal)
IV tPA for Acute Ischemic Stroke
     ~Exclusion Criteria
70
        Suspected SAH despite a normal CT scan
        Gastrointestinal or urinary tract hemorrhage within 21 d
        Arterial puncture at a noncompressive site within 7 d
        Seizure at the onset of stroke with uncertain new stroke
        Use of heparin within 48 h and an elevated PTT-aPTT
        Old stroke with diabetes mellitus
        Use of warfarin and INR >1.7
        Platelet count < 100,000/mm3
        Glucose < 50 or > 400 mg/dL
Guidelines for IV thrombolysis
     ~ Care during the first 24 hours after administration of
     tPA
71
        Admission to a skilled care facility (ICU or acute stroke unit)
        Careful monitor and management of BP
              Keep SBP<185 mmHg, DBP<110 mmHg
        No use of anticoagulants and antiplatelet
        Central venous access and arterial punctures are restricted
        Placement of an indwelling bladder catheter should be avoided
         during drug infusion and for at least 30 minutes after infusion
         ends
        Insertion of a nasogastric tube should be avoided
        Careful neurological evaluation (NIHSS at 1st, 2nd, 24th hours)
Risk of hemorrhagic changes
72

        Marked hyperglycemia              Higher NIHSS score
         or DM                             Longer time to
        CT >1/3 MCA                        recanalization
        Increasing stroke                 Lower platelet counts
         severity                          Higher glucose level at
        Low platelet counts                admission


                  ~ Circulation. 2002                    ~ Stroke. 2002
Guidelines for IV Thrombolysis
     ~ Bleeding Management
73
        Head CT should be obtained on an emergent basis whenever
         neurological worsening (NIHSS increase >4)
        Any life-threatening hemorrhagic complication, including
         ICH, should be followed by these sequential steps:
            Discontinue ongoing infusion of thrombolytic drug
            Obtain blood samples for coagulation tests
               HCT,    HB, PT/INR, PTT, PLT, Blood type
            Obtain surgical consultation, as necessary
            Consider other interventions that may be useful, such as transfusion
              4  units packed RBC, 2 units FFP, 6 units
                cryoprecipitate, 1 unit PLT
IV rt-PA in Acute Ischemic Stroke
  Case Presentation




72 female, HT, CAD, AF, Sudden left hemiplegia
Initial NIHSS (1 hour): 19
NIHSS 1 week later: 8
Hemorrhagic transformation (asymptomatic) of right MCA territory
IV rt-PA in Acute Ischemic Stroke
    Case Presentation




65 year-old female, no known major systemic diseases
Acute onset, left hemiplegia, neglect, and hemianopia.
ER arrival in 1 hour. Initial NIHSS: 15
24 hours after IV-tPA therapy: NIHSS: 3
Discharge (10 days later): NIHSS: 0, mRS: 0, Barthel index: 100
Intra-arterial Thrombolysis
76

                                       M2 superior division
            Microcatheter   Thrombus




                            MCA, M1



      ICA                                M2 inferior division
Intra-arterial Thrombolysis
77
Intra-arterial Thrombolysis
78
        Advantage
            Higher recanalization rate
            Symptomatic brain hemorrhage
                 8.3% in the carotid system
                 6.5% in vertebrobasilar territory
                 No higher than those in IV thrombolysis
        Disadvantage
            Ready availability of neuro-interventionalists, a stroke
             team, and a stroke ICU
            Additional time required to begin treatment compared to
             IV thrombolysis
Mechanical Clot Disruption and Removal
 –   121 patients with MCA infarct less than 6 h
 –   Some also received IA thrombolysis
 –   Median NIHSS was 19, 40% had baseline NIHSS >20
 –   114 were treated with MERCI device
 –   Recanalization rate: 54%
 –   Symptomatic brain hemorrhage: 8%
      • 5% with retriever alone, 24% with retriever and IA thrombolysis
 – Mortality at 3 mo: 40%
                                                                          Stroke 2005;36:1432-8.

                                                  After the microcatheter transverses the thrombus,
                                                  the first loops of the Merci Retriever are delivered
                                                  distal to the occlusion site.

                                                  The Merci Retriever is pulled back at the contact
                                                  of the thrombus, additional loops are delivered within
                                                  the thrombus, and the Merci Retriever is torqued to
                                                  ensnare the thrombus.

                                                  The balloon of the balloon guide catheter (BGC)
                                                  (insert) is inflated to control antegrade flow, and
                                                  the Merci Retriever is pulled back with the ensnared
                                                  thrombus toward the tip of the BGC where it is
                                                  aspirated.
Ultrasound-Enhanced Thrombolysis
80
        Intra-venous rt-PA thrombolysis and continuous 2-MHz
         transcranial Doppler ultrasonography <3 hours after stroke onset
        Augment arterial recanalization
        Increased neurological recovery




                                        Alexandrov A et al. N Engl J Med 2004;351:2170-2178
Future Treatment of Acute Ischemic
     Stroke
81
        New thrombolytic agents
        Combined IV+IA thrombolysis
            IV tPA within 3 h, IA tPA 3-6 h
        Combined thrombolytic agents and antiplatelets
        Combined thrombolytic agents and anticoagulant
        Neuroprotection agents
        MRI diffusion-perfusion mismatch
            3-9 h after stroke onset
        Clot/thrombus retrieval
Ischemic Penumbra
Current available antithrombotic agents
                for acute ischemic stroke
83
        Oral antiplatelet agents            Heparins
            Aspirin                             Unfractionated heparin
            Ticlopidine                         Low-molecule-weight
            Clopidogrel
                                                  heparins
            Dipyridamole                             Dalteparin
            Aspirin + extended-release               Enoxaparin
             dipyridamole
            Cilostazol
                                                      Tinzaparin
                                             Heparinoids
        Glycoprotein IIb/IIIa                   Danaparoid
         inhibitors
            Abciximab
                                             Direct thrombin
            Tirofiban                        inhibitors
            Epifibatide                         Argatroban
                                                 Bivalirudin
                                                 Lepirudin
Antiplatelet in Acute Ischemic
                          Stroke
84
        International Stroke Trial (IST)
            19,436 patients, ASA 300 mg/day, <48 hors

        Chinese Acute Stroke Trial (CAST)
            21,106 patients, ASA 160 mg/day, <48 hours

        Combined analysis of ASA vs placebo
            Absolute risk reduction reduction of deaths or nonfatal stroke:
             0.9%
            Absolute risk reduction reduction of early stroke recurrence:
             0.7%
            Small increase in ICH or systemic hemorrhage: IST (1.1% vs
             0.6%), CAST (0.8% vs 0.6%)
                                                         Stroke 2002;33:1934-42
Effect of various therapies for treatment
           of acute ischemic stroke
Agent        Trial   Outcome                             Effect
Aspirin      IST     Hemorrhagic stroke at 2 wk          Harm of 1 per 1000 (NS)
                     Death or nonfatal stroke at 2 wk    Benefit of 11 per 1000 (p<0.05)
                     Dead or dependent at 6 mo           Benefit of 13 per 1000 (p=0.07)
             CAST    Hemorrhagic stroke at 2 wk          Harm of 2 per 1000 (NS)
                     Death or nonfatal stroke at 1 mo    Benefit of 7 per 1000 (p=0.03)
                     Dead or dependent at 1 mo           Benefit of 11 per 1000 (p=0.08)
Heparin      IST     Recurrent ischemic stroke at 2 wk   Benefit of 9 per 1000 (p<0.01)
(any dose)           Hemorrhagic stroke at 2 wk          Harm of 8 per 1000 (p<0.0001)
                     Major extracranial hemorrhage       Harm of 9 per 1000 (p<0.0001)
                     Pulmonary embolism                  Benefit of 3 per 1000 (p<0.05)
                     Death or nonfatal stroke at 2 wk    Benefit of 4 per 1000 (NS)
                     Dead or dependent at 6 mo           No effect (NS)
Heparin      IST     Recurrent ischemic stroke at 2 wk   Benefit of 12 per 1000 (p<0.001)
5000 U bid           Hemorrhagic stroke at 2 wk          Harm of 3 per 1000 (p<0.05)
                     Major extracranial hemorrhage       Harm of 2 per 1000 (NS)
                     Pulmonary embolism                  Benefit of 12 per 1000 (NS)
                     Death or nonfatal stroke at 2 wk    Benefit of 12 per 1000 (p<0.05)
                     Dead or dependent at 6 mo           Harm of 2 per 1000 (NS)
Antithrombotics for Stroke Prevention
86
        Primary stroke prevention
            Ischemic stroke prevention
                Antiplatelets: aspirin, others
            Cardioembolic stroke prevention
                Anticoagulants: warfarin, others

        Secondary stroke prevention
            Ischemic stroke prevention
                Antiplatelets: aspirin, dipyridamole, ticlopidine, clopidogrel,
                 glycoprotein IIb/IIIa receptor antagonist
            Cardioembolic stroke prevention
                Anticoagulants: heparin, warfarin, others
Decision-making of antithrombotic therapy for
     acute ischemic stroke
87
                   Suspected acute                                                     No antithrombotic
                   ischemic stroke                   Head CT
                                                                    Not completed           therapy
                                                                    or reveals ICH
                                           Yes        Eligible
                   Administer t-PA
                                                     for t-PA?
                                                                    Aspirin intolerance
                                                      No              or high risk of
                                                                     recurrent stroke Clopidogrel 75 mg/day
                      Head CT                    ASA 160-300 mg                            or ASA 25 mg +
                     at 24 hours
                                                                                       dipyridamole 200 mg bid

                                                       Rapid
                                                     diagnostic
                                                     evaluation


         Cardioembolism               Large artery         Small artery        Arterial         Cryptogenic
                                   atherothrombosis         occlusion         dissection        ASA 100 mg/d
       Consider anticoagulation
                                   Consider ASA,           ASA 100 mg/d     Consider ASA,
       Warfarin, INR 2-3 If
                                   clopidogrel, or                          ? anticoagulation
       no contraindication,
       Extreme high risk           ASA+dipyridamole
       Consider UFH or             ? anticoagulation
       LMWH


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Manage ischemic stroke pts

  • 1. 1 Management of Acute Ischemic Stroke Patients Jiann-Shing Jeng, MD, PhD Stroke Center & Department of Neurology National Taiwan University Hospital, Taipei, Taiwan
  • 2. Stroke Types: NTUH, 1995~2007 2 Large artery atherosclerosis 12% Small artery lacune Subarachnoid 22% hemorrhage 6% Cardioembolism 14% Cerebral hemorrhage Other determined 22% Undetermined 4% 20%
  • 3. Stroke Chain of Survival 3  Detection Recognition of stroke signs/symptoms  Dispatch Call 119 and priority EMS dispatch  Delivery Prompt transport and prehospital notification to hospital  Door Immediate ED triage  Data ED evaluation, prompt laboratory studies, and CT imaging  Decision Diagnosis and decision about appropriate therapy  Drug Administration of appropriate drugs or other intervention
  • 4. EMS in Acute Stroke 4  Rapid identification of acute stroke  Elimination of comorbid conditions mimicking stroke  Stabilization  Rapid transportation  Notification of receiving institution
  • 5. Prehospital Stroke Identification 5  Los Angeles Prehospital Stroke Screening  Cincinnati Prehospital Stroke Scale
  • 6. Los Angeles Prehospital Stroke Screen (LAPSS) 6  Last time patient known to be symptom free  Screening criteria 1. Age >45 y 2. No history of seizure or epilepsy 3. Symptom duration less than 12 hours 4. No previously bedridden or wheelchair bound 5. Blood glucose 60-400 mg/Dl 6. Exam:  Facial smile/grimace: normal, droop  Grip: normal, weak grip, no grip  Arm strength: normal, drifts down, falls rapidly
  • 7. LOS ANGELES MOTOR SCALE (LAMS) 7 Normal Right Left Total Facial Ͱ Droop (1) Ͱ Droop (1) Ͱ (0) smile/grimace Ͱ Weak grip (1) Ͱ Weak grip (1) Grip Ͱ (0) Ͱ No grip (2) Ͱ No grip (2) Ͱ (0) Ͱ Drifts down (1) Ͱ Drifts down (1) Arm strength Ͱ Falls rapidly (2) Ͱ Falls rapidly (2) TOTAL Score
  • 8. Cincinnati Prehospital Stroke Scale 8  Facial droop  Normal : both sides of face more equally  Abnormal : one side of face does not move as well as the other  Arm drift  Normal : both arms move the same or both arms do not move at all  Abnormal : one arm either does not move or drift down compared to the other  Speech  Normal : says correct words with no slurring  Abnormal : slurs words, says the wrong words, or is unable to speak
  • 9. How to approach a patient with probable acute stroke? 9  New onset of acute  Subsequent hospital neurological deficit management  Differential diagnosis of other  Acute stroke non-stroke diseases management  Establish cause of  Initial ER assessment and stroke management  Stroke risk factors  Vital signs, sugar  Dysphagia screening  Consciousness: GCS  Early rehabilitation  Non-contrast head CT  PT, OT, ST  Stroke severity: NIHSS  Plan for secondary  Stroke type and location prevention of stroke  Hyperacute management Thrombolytic therapy Craniectomy Intensive care/monitoring
  • 10. History for initial diagnosis of acute stroke 10  Rapid, accurate history taking  Often from the family members  Key elements of history  Onset time: the last time of normal neurological status  Onset mode: sudden, acute, subacute  Onset symptoms: focal or generalized symptoms  Course: progression of symptoms  Co-morbid diseases: HTN, DM, Heart diseases, etc.  Use of medications: antiplatelets, anticoagulants, antihypertensives, insulin, etc.
  • 11. Misdiagnosis of Acute Stroke ~ NTUH experience 11 No. % Acute stroke 2226 87.6 Misdiagnosis of acute stroke 316 12.4 Possible neurovascular disorders 57 2.2 Other neurological disorders 209 8.2 Non-neurological disorders 50 2.0 Total 2542 100.0
  • 12. Differential Diagnosis of Acute Stroke 12  Old cerebrovascular disease  Craniocerebral/cervical trauma  Meningitis/encephalitis  Hypertensive encephalopathy  Intracranial mass (tumor, subdural/epidural hematoma)  Seizure with persistent neurological signs (Todd’s paralysis)  Vestibulopathy  Spinal cord or peripheral nerve lesions  Migraine with persistent neurological signs  Metabolic:  Hyperglycemia  Hypoglycemia  post-cardiac arrest hypoxia  Infection  Drug overdose, etc.
  • 13. NTUH ER Stroke Assessment: History 13 Stroke/TIA Onset Time: 確定 年 月 日 時 分 不確定 Stroke/TIA Onset Symptoms: drowsiness, stupor, delirium, coma, headache, vomiting, neck stiffness, seizures, anopia, aphasia ( sensory, motor), apraxia, vertigo, dizziness, dysarthria, dysphagia, diplopia, ataxia, incontinence left side weakness ( face, upper limb, lower limb), right side weakness ( face, upper limb, lower limb), left side numbness ( face, upper limb, lower limb), right side numbness ( face, upper limb, lower limb), Others: Stroke/TIA Onset Mode: sudden, acute, fluctuating course Activity at Stroke/TIA Onset: strenuous activity, ordinary activity, rest, sleep Stroke in Progression: yes (symptoms progression>1 hour), no
  • 14. NTUH ER Stroke Assessment: NIHSS 14 1a. Level of Consciousness (LOC) 4. Facial Palsy 7. Limb Ataxia □ 0= Alert □ 0= Normal □ 0= Absent □ 1= Not alert, but arousable □ 1= Minor □ 1= Present in one limb. □ 2= Not alert, obtunded □ 2= Partial □ 2= Present in two limbs □ 3= Uunresponsive □ 3= Complete 8. Sensory 1b. LOC Questions 5a Left Motor Arm □ 0= Normal □ 0= Answers both questions □ 0= No drift □ 1= Mild to moderate sensory loss correctly □ 1= Drift □ 2= Severe □ 2= Some effort against gravity □ 1= Answers one question correctly 9. Best Language □ 3= No effort against gravity □ 2= Answers neither question □ 4= No movement □ 0= normal correctly 5b. Right Motor Arm □ 1= Mild to moderate aphasia 1c. LOC Commands □ 0= No drift □ 2= Severe aphasia □ 0= Performs both tasks correctly □ 1= Drift □ 3= Mute, global aphasia □ 1= Performs one task correctly □ 2= Some effort against gravity 10. Dysarthria □ 2= Performs neither task correctly □ 3= No effort against gravity □ 0= Normal 2. Best Gaze □ 4= No movement □ 1= Mild to moderate □ 0= Normal 6a. Left Motor Leg □ 2= Severe □ 1= Partial gaze palsy □ 0= No drift 11. Extinction and Inattention □ 2= Forced deviation or total gaze □ 1= Drift □ 0= Normal paresis □ 2= Some effort against gravity □ 1= One sensory modality 3. Visual □ 3= No effort against gravity □ 2= More than one sensory modality □ 0= No visual loss □ 4= No movement □ 1= Partial hemianopia. 6b. Right Motor Leg □ 2= Complete hemianopia □ 0= No drift Total Score: □ 3= Bilateral hemianopia □ 1= Drift □ 2= Some effort against gravity □ 3= No effort against gravity □ 4= No movement
  • 15. NTUH ER Stroke Assessment: Diagnosis 15 Head CT Findings: □Hemorrhage □Ischemia Early sign: Diagnosis: □Ischemic Stroke (□ left, □right ) □ACA; □MCA, total; □MCA, partial; □PCA; □Brainstem, □cerebellum □Hemorrhagic Stroke (site: ) □Others: Management Suggestion:
  • 16. Head images for acute stroke diagnosis 16 Everyone with suspected stroke  CT without contrast Some patients required stroke mechanism realization or treatment consideration  MRI  MRA  CTA  Ultrasound (duplex, transcranial Doppler, Echocardiography)  Conventional angiography
  • 17. Early CT signs in acute MCA stroke 17 Left and middle: Hyperdense left MCA sign (yellow arrow), hypoattenuated left basal ganglia (red arrow), and cortical swelling (blue arrows) in the same patient. Right: Dot sign (yellow arrow) in the left sylvian fissure.
  • 18. Alberta Stroke Program Early CT Score (ASPECTS)  Quantify the extent of CT hypodensity in acute stroke A M1 C I L M2 IC M3 P Barber et al. Lancet. 2000;355:1670-4.
  • 19. Diagnosis of Acute Stroke 19  Stroke vs. non-stroke  Infarction or hemorrhage  Infarction  Location diagnosis  Arterial territory diagnosis  Pathophysiology diagnosis  Etiology diagnosis
  • 20. Location Diagnosis of Stroke 20  Supratentorial site  Hemisphere side  Cortical or subcortical areas  Frontal, parietal, temporal lobe  Infratentorial site  Midbrain, pons, medulla, cerebellum
  • 21. Arterial Territory Diagnosis of Stroke 21  ICA: more than MCA territory  ACA  MCA  Lenticulostriate artery  Cortical branches  Internal borderzone area  PCA  External borderzone area  V-B system  Extracranial VA  Intracranial  VA, BA, PICA, AICA, SCA
  • 22. Acute Stroke Case 22 A 70-year-old, right-handed man has been known to have previous history of poorly controlled hypertension, diabetes, and cardiac arrhythmia. He developed abrupt onset of left-sided weakness after dinner at 7 pm. What should you do?
  • 23. Acute Stroke Case 23 He brought to a medical center ER by the EMS at 8:30 pm. On initial ER arrival, his consciousness was awake, blood pressure was 210/120 mmHg, pulse rate was 120/min irregularly, respiratory rate was 20/min, body temperature was 37°C and blood sugar was 320 mg/dL. What should you do if you are on duty at ER ?
  • 24. Acute Stroke Case 24 Neurologically, he had flaccid hemiplegia and right- sided gaze preference with dense left-sided hemineglect. The NIHSS score was 17. Head CT scan revealed effacement of cortical sulcal marking in the right middle cerebral artery territory and hyperdense MCA sign. What is your diagnosis of the stroke ? What are the next you will do ?
  • 25. Diagnosis of Acute Stroke 25  Stroke  confirmed by history and images  Infarction  confirmed by head CT  Location  right MCA territory (>1/2)  Arterial territory  right MCA, main trunk  Pathophysiology  embolism  Etiology  cardioembolism, atrial
  • 26. Arterial Occlusion Embolism Site Microembolus Atheroma
  • 27. Stroke Evaluation Targets for Potential Thrombolytic Candidates 27 Time Target Door to doctor 10 minutes Door to CT completion 25 minutes Door to CT read 45 minutes Door to treatment 60 minutes Assess to neurological expertise 15 minutes Assess to neurosurgical expertise 2 hours Admit to monitored bed 3 hours
  • 28. Acute Ischemic Stroke Protocol 28 ER arrival Triage nurse confirm stroke onset time < 4 hours ER Resident performs Rapid evaluation (5 minutes) Neurology Resident receives 1.exact time of onset ER stroke page and 2.important history proceeds to ER 3.quick neurological evaluation brief history & physical exam STAT CT and blood work Page Stroke VS Head CT findings, laboratory data, NIH stroke scale Confirm the criteria fulfilling thrombolytic therapy for ischemic stroke Family’s agreement for thrombolytic therapy Stroke onset < 3 hours Stroke onset 3-6 hours Call Neuroradiologists IV-tPA treatment IA thrombolytic therapy IA thrombolysis Patient is admitted to Stroke ICU for intensive monitoring/care
  • 29. Essentials of Acute Stroke Care 29  Acute stroke team  Multi-disciplinary care  Stroke units  Intensive care of stroke patients  Standardized protocol of acute stroke management  Early rehabilitation of acute stroke patients
  • 30. Acute Stroke Teams 30  Acute stroke team consists of health care professional with experience and expertise in stroke  Available 24 hours everyday, within 15 minutes of the call  At a minimum, a qualified acute stroke physician and another health care professional
  • 31. Stroke Units 31  A setting designed for the care of stroke  Admission/discharge criteria, patient census and outcome data  Staffed and directed by personnel (physicians, nurses, etc.) with training and expertise in caring for patients with cerebrovascular disease  Equipment and written protocols for stroke patient care: Neuro, Cardiac, B/P monitoring
  • 32. Potential Benefits of Stroke Units 32 50 Cases saved from death and dependency 45 40 35 per 1,000 events 30 25 20 15 10 5 0 Stroke unit ASA tPA <3h tPA <6h Neuroprotective agents Gilligan et al. Cerebrovasc Dis. 2005;20:239-44.
  • 33. Goal of Acute Ischemic Stroke Care 33 Treatment goals Therapeutic strategies To reverse brain ischemia before it cause Recanalization, esp. permanent brain injury thrombolysis To prevent stroke in evolution and recurrence Antithrombotic agents To optimize the patient’s medical condition and Homeostasis of the brain prevent the common medical sequelae that occur after stroke or after a stroke intervention To optimize functional recovery after the Early rehabilitation residual permanent injury that has occurred
  • 34. Homeostasis of the Brain 34  Blood pressure  SBP 120-220 mmHg, DBP 70- 110 mmHg  Blood glucose level  blood sugar 100-150 mg/dL  Body temperature  <37.5°C  Oxygen saturation  >95%
  • 35. Blood Pre s s ure in Ac ute Is c he mic S troke 35  A spontaneous increase in BP is common in patients with acute ischemic stroke, and the increase in BP tends to be more pronounced in patients with preexisting hypertension.  Elevations in systolic blood pressure >160 mm Hg are detected in 60% of patients with acute stroke.
  • 36. C aus e of Ele vate d Blood Pre s s ure in Ac ute S troke 36  Stress of hospitalization  Stress of the cerebrovascular event  A full bladder, nausea, pain, other body discomfort  Preexisting hypertension  A physiological response to hypoxia  A response to increased intracranial pressure
  • 37. Blood Pre s s ure in Ac ute Is c he mic S troke 37  In a majority of patients, BP tends to decline in the first few days to weeks after stroke onset, even without pharmacological intervention.  A significant decline in BP can be seen in approximately a third of patients in the first few hours after stroke onset.
  • 38. Blood Pre s s ure in Ac ute Is c he mic S troke 38  BP often falls spontaneously when the patient is moved to a quiet room, the patient is allowed to rest, the bladder is emptied, or the pain is controlled.  In addition, treatment of increased intracranial pressure may result in a decline in BP.
  • 39. Time course of blood pressure (MAP) with acute ischemic stroke 39 Christensen et al. Acta Neurol Scand 2002;106:142-7.
  • 40. Admission Blood Pressure and Outcome ~ International Stroke Trial 40 Leonardi-Bee et al. Stroke 2002;33:1315-20.
  • 41. High Blood Pressure in Acute Stroke and Outcome 41  For every 10-mm Hg increase >180 mm Hg, the risk of neurological deterioration increased by 40% and the risk of poor outcome increased by 23%
  • 42. Cerebral Perfusion Pressure 42  Cerebral perfusion pressure (CPP) = Mean arterial blood pressure (MABP) – intracranial pressure (ICP)  Maintain CPP >60 mm Hg to ensure cerebral blood flow  In case of elevated ICP, elevated BP is required for maintaining adequate CPP.
  • 43. Management of Elevated BP in Acute Ischemic Stroke 43  Current recommendation based on the type of stroke  Antihypertensive therapy in acute ischemic stroke  Aggressive antihypertensive therapy may lower the cerebral perfusion pressure and lead to stroke worsening  Acute stroke patient may have exaggeration of response to antihypertensive agents  For nonthrombolytic candidates Not to treat if SBP <220, DBP <120, or MAP <130 mm Hg.  For thrombolyic candidates Not to treat if SBP <185, or DBP <110 mm Hg
  • 44. BP Lowe ring in Ac ute Is c he mic s troke 44  When treatment is indicated, lowering the BP should be done cautiously.  Some strokes may be secondary to hemodynamic factors, and a declining BP may lead to neurological worsening.
  • 45. Blood Pressure Management of Ischemic Stroke (nonthrombolytic candidates) 45 Blood pressure Treatment DBP >140 mm Hg Sodium nitroprusside (0.5 ug/kg/min). Aim for 10-20% reduction in DBP. SBP >220, DBP >120, or 10-20 mg labetalol IV push over 1-2 min. MAP >130 mm Hg May repeat or double labetalol every 20 min to a maximum dose of 150 mg. SBP <220, DBP <120, or Emergent antihypertensive therapy is MAP <130 mm Hg deferred in the absence of aortic dissection, acute myocardial infarction, severe congestive heart failure, or hypertensive encephalopathy
  • 46. Intravenous Medications Considered for Control of Elevated BP in Patients With ICH ~ AHA, 2007 46 Drug Bolus Dose Continuous Infusion Rate Labetalol 5~20 mg every 15 min 2 mg/min (maximum 300 mg/d) Nicardipine NA 5~15 mg/h Esmolol 250 μg/kg IV push loading dose 25~300 μg/kg/min Enalapril 1.25~5 mg IV push every 6 h* NA Hydralazine 5~20 mg IV push every 30 min 1.5~5 μg/kg/min Nipride NA 0.1~10 μg/kg/min Nitroglycerin NA 20~400 μg/min Broderick et al. Stroke. 2007;38.
  • 47. Common Intravenous Anti- Hypertensive Drugs Use in ICU 47  Sodium Nitroprusside (Nipride)  Direct vasodilation  Labetalol (Trandate)  β and α-1 blockade  Nicardipine (Perdipine)  Calcium channel blockade
  • 48. Sodium Nitroprusside 48 Mechanism : Direct artery and vein dilation Administration : IV infusion Onset : Seconds Duration : Continuous, during infusion Advantage : Balanced ↓ of preload & afterload Disadvantage : 1. Excessive hypotension 2. Reflex tachycardia 3. Light sensitivity 4. Potential cyanide/thiocyanate toxicity Dosage : 0.25-10 µg/kg/min IV
  • 49. Labetalol 49 Mechanism : β and α-1 blockade Administration : Bolus/infusion Onset : bolus -- 5~30 min, infusion -- 15~60 min Duration : 2~12 hrs Advantage : 1. Little change in HR and CO 2. Intra-A or ICU monitoring (-) Disadvantage : 1. Orthostatic hypotension 2. Urinary retention 3. β-blocker’s contra-indications Dosage : 10-80 mg IV q10 min up to 300 mg, IV infusion: 0.5-2 mg/min
  • 50. Nicardipine 50 Mechanism : Calcium blockade, endothelin-1 antagonism Administration : Bolus/infusion Onset : 1-5 min Duration : 3~6 hrs Advantage : 1. no interference with CBF, CO 2. diuretic effect 3. inhibit platelet aggregation, vasospasm Disadvantage : 1. hypotension 2. bradycardia Dosage : 5 mg/h IV, 2.5 mg/h q15 min, up to 15 mg/h
  • 51. Blood Glucose within the first 48 hours after stroke 51  124 patients with ischemic stroke without previously diagnosed diabetes had blood glucose measured at least 4-hourly until 48 hours poststroke.  The mean glucose was 6.6 mmol/L throughout the period of monitoring, with no change over time.  More severe stroke and glucose-lowering therapy to be associated with higher poststroke glucose levels. Wong et al. Neurology 2008;70:1036-41.
  • 52. Poststroke Hyperglycemia 52  Persistent hyperglycemia  Definition: mean blood glucose >7 mmol/L (126 mg/dL) or HbA1C >6.2%  An independent determinant of infarct expansion  Associated with worse functional outcome Baird al. Stroke. 2003;34:2208-14.
  • 53. Intensive Insulin Therapy in the Medical ICU 53  A prospective, randomized, controlled study of 1,200 adult patients admitted to the medical ICU.  Comparison between conventional therapy (insulin administered when blood glucose >215 mg/dL) and intensive therapy (blood glucose control within 80-110 mg/dL)  Intensive insulin therapy significantly reduced morbidity among all patients in the medical ICU. Van den Berghe et al. N Engl J Med. 2006;354:449-61.
  • 54. Respiratory Failure in Acute Stroke Patients 54  Major causes  Prognosis: poor in  Aspiration pneumonia 49-93%  Impaired central respiratory drive  Respiratory function  Neurogenic pulmonary  Risk for aspiration, edema airway obstruction,  Overall stroke: 10% hypoventilation.  Ischemic stroke: 5-6%  Target at O2  ICH: 26-30% saturation > 95%  SAH: 47%
  • 55. Fever and ischemic stroke 55  Fever correlates with increased severity of stroke, mortality, and poorer prognosis in patients with ischemic stroke  Differentiation of the fever causes  central, drug, infection, etc.  Hyperthermia  May accelerate cerebral metabolism and neuronal injury  A marker of severity of stroke or a consequence of large strokes is unclear  Mild hypothermia  Improve neurological outcome  Reduce elevated ICP
  • 56. Causes of Intracranial Hypertension 56  Intracranial mass  Cerebral edema  Cytotoxic (intracellular)  Vasogenic (extracellular)  Cerebrospinal fluid hypervolemia  Decreased absorption  Overproduction of CSF  Increased intracranial blood volume  Cerebral vasodilatation (hypoxia, hypercapnia)  Obstructed venous outflow
  • 57. IICP Management in Acute Ischemic Stroke 57 General  Osmotherapy  cardiopulmonary and  Mannitol metabolic support  Glycerol  Positioning:elevate head of  Hypertonic saline the bed to 30o  Hyperventilation  Treat fever  Surgery  Treat seizure  Drainage of  Avoidhypoxia and cerebrospinal fluid: hypercapnia ventriculostomy, VP shunt  Avoid hypo-osmolar fluids  Craniectomy  Avoid hyperglycemia
  • 58. Medical Therapy in Acute Ischemic Stroke 58  Thrombolytic therapy  IV rt-PA therapy  IA rt-PA or urokinase therapy  Combined IV and IA thrombolysis  Antithrombotic therapy  Antiplatelets: aspirin, clopidogrel (Plavix), Aggrenox  Anticoagulants: heparin, low-molecular weight heparin, warfarin  Neuroprotection: uncertain effect
  • 59. Territory infarct vs. borderzone infarct 59
  • 60. Penumbrae of Ischemic Stroke 60  Penumbrae is the target of any reperfusion therapy  The fate of brain tissue depends on  Time  Cerebral blood flow  Occluded arterial flow  Collateral blood flow  Time is brain
  • 61. Outcomes in rt-PA-treated Patients Compared with Controls at 3 M After Stroke 61 NINDS rt-PA Study Group. NEJM 1995;333:
  • 62. IV Thrombolysis of Acute Ischemic Stroke ~ Cochrane Meta-Analysis 62 death or dependency (mRS 3-6) death or dependency (mRS 3-6) treated up to 3 h after stroke treated up to 6 h after stroke
  • 63. Model Etimating OR for Favourable Outcome at 3 M in rt-PA-treated Patients Compared with Controls 63 Hacke et al. Lancet 2004;363:768-774
  • 64. Cochrane thrombolysis meta-analysis symptomatic (including fatal) intracranial hemorrhage 64
  • 65.  Outcome in SITS-MOST and Pooled Randomised Controlled Trials at 3 M After Stroke Onset 65 Wahlgren et al. Lancet 2007;369:275-82.
  • 66. ECASS III : IV rt-PA 3~4.5 hours Distribution of Scores on the Modified Rankin Scale 66 Hacke et al. N Engl J Med. 2008;359:1317-29.
  • 67. ECASS III : IV rt-PA 3~4.5 hours Odds Ratios for Functional End Points at Days 90 and 30 after Treatment 67 Hacke et al. N Engl J Med. 2008;359:1317-29.
  • 68. IV tPA for Acute Ischemic Stroke ~ Inclusion Criteria 68  Ischemic stroke with clearly defined symptom onset  Measurable deficit on the NIH Stroke Scale  Age >18 years  No evidence of intracranial blood on the brain CT scan  Timing from the symptom onset to initiate of IV rt-PA  NINDS (1995) : <3 hours  ECASS-III (2008) : <4.5 hours
  • 69. IV tPA for Acute Ischemic Stroke ~Exclusion Criteria 69  Rapidly improving or minor stroke symptoms (NIHSS <4)  Severe stroke symptoms by clinical (e.g., NIHSS >25) or head CT scan (> 1/3 MCA low density)  Stroke or serious head trauma within 3 mo  Major surgery within 14 d  History of intracranial hemorrhage  Systolic BP >185 mmHg or diastolic BP >110 mmHg of treatment initiation  Aggressive BP treatment (i.e., continuous IV infusion of antihypertensive to achieve above goal)
  • 70. IV tPA for Acute Ischemic Stroke ~Exclusion Criteria 70  Suspected SAH despite a normal CT scan  Gastrointestinal or urinary tract hemorrhage within 21 d  Arterial puncture at a noncompressive site within 7 d  Seizure at the onset of stroke with uncertain new stroke  Use of heparin within 48 h and an elevated PTT-aPTT  Old stroke with diabetes mellitus  Use of warfarin and INR >1.7  Platelet count < 100,000/mm3  Glucose < 50 or > 400 mg/dL
  • 71. Guidelines for IV thrombolysis ~ Care during the first 24 hours after administration of tPA 71  Admission to a skilled care facility (ICU or acute stroke unit)  Careful monitor and management of BP  Keep SBP<185 mmHg, DBP<110 mmHg  No use of anticoagulants and antiplatelet  Central venous access and arterial punctures are restricted  Placement of an indwelling bladder catheter should be avoided during drug infusion and for at least 30 minutes after infusion ends  Insertion of a nasogastric tube should be avoided  Careful neurological evaluation (NIHSS at 1st, 2nd, 24th hours)
  • 72. Risk of hemorrhagic changes 72  Marked hyperglycemia  Higher NIHSS score or DM  Longer time to  CT >1/3 MCA recanalization  Increasing stroke  Lower platelet counts severity  Higher glucose level at  Low platelet counts admission ~ Circulation. 2002 ~ Stroke. 2002
  • 73. Guidelines for IV Thrombolysis ~ Bleeding Management 73  Head CT should be obtained on an emergent basis whenever neurological worsening (NIHSS increase >4)  Any life-threatening hemorrhagic complication, including ICH, should be followed by these sequential steps:  Discontinue ongoing infusion of thrombolytic drug  Obtain blood samples for coagulation tests  HCT, HB, PT/INR, PTT, PLT, Blood type  Obtain surgical consultation, as necessary  Consider other interventions that may be useful, such as transfusion 4 units packed RBC, 2 units FFP, 6 units cryoprecipitate, 1 unit PLT
  • 74. IV rt-PA in Acute Ischemic Stroke Case Presentation 72 female, HT, CAD, AF, Sudden left hemiplegia Initial NIHSS (1 hour): 19 NIHSS 1 week later: 8 Hemorrhagic transformation (asymptomatic) of right MCA territory
  • 75. IV rt-PA in Acute Ischemic Stroke Case Presentation 65 year-old female, no known major systemic diseases Acute onset, left hemiplegia, neglect, and hemianopia. ER arrival in 1 hour. Initial NIHSS: 15 24 hours after IV-tPA therapy: NIHSS: 3 Discharge (10 days later): NIHSS: 0, mRS: 0, Barthel index: 100
  • 76. Intra-arterial Thrombolysis 76 M2 superior division Microcatheter Thrombus MCA, M1 ICA M2 inferior division
  • 78. Intra-arterial Thrombolysis 78  Advantage  Higher recanalization rate  Symptomatic brain hemorrhage  8.3% in the carotid system  6.5% in vertebrobasilar territory  No higher than those in IV thrombolysis  Disadvantage  Ready availability of neuro-interventionalists, a stroke team, and a stroke ICU  Additional time required to begin treatment compared to IV thrombolysis
  • 79. Mechanical Clot Disruption and Removal – 121 patients with MCA infarct less than 6 h – Some also received IA thrombolysis – Median NIHSS was 19, 40% had baseline NIHSS >20 – 114 were treated with MERCI device – Recanalization rate: 54% – Symptomatic brain hemorrhage: 8% • 5% with retriever alone, 24% with retriever and IA thrombolysis – Mortality at 3 mo: 40% Stroke 2005;36:1432-8. After the microcatheter transverses the thrombus, the first loops of the Merci Retriever are delivered distal to the occlusion site. The Merci Retriever is pulled back at the contact of the thrombus, additional loops are delivered within the thrombus, and the Merci Retriever is torqued to ensnare the thrombus. The balloon of the balloon guide catheter (BGC) (insert) is inflated to control antegrade flow, and the Merci Retriever is pulled back with the ensnared thrombus toward the tip of the BGC where it is aspirated.
  • 80. Ultrasound-Enhanced Thrombolysis 80  Intra-venous rt-PA thrombolysis and continuous 2-MHz transcranial Doppler ultrasonography <3 hours after stroke onset  Augment arterial recanalization  Increased neurological recovery Alexandrov A et al. N Engl J Med 2004;351:2170-2178
  • 81. Future Treatment of Acute Ischemic Stroke 81  New thrombolytic agents  Combined IV+IA thrombolysis  IV tPA within 3 h, IA tPA 3-6 h  Combined thrombolytic agents and antiplatelets  Combined thrombolytic agents and anticoagulant  Neuroprotection agents  MRI diffusion-perfusion mismatch  3-9 h after stroke onset  Clot/thrombus retrieval
  • 83. Current available antithrombotic agents for acute ischemic stroke 83  Oral antiplatelet agents  Heparins  Aspirin  Unfractionated heparin  Ticlopidine  Low-molecule-weight  Clopidogrel heparins  Dipyridamole  Dalteparin  Aspirin + extended-release  Enoxaparin dipyridamole  Cilostazol  Tinzaparin  Heparinoids  Glycoprotein IIb/IIIa  Danaparoid inhibitors  Abciximab  Direct thrombin  Tirofiban inhibitors  Epifibatide  Argatroban  Bivalirudin  Lepirudin
  • 84. Antiplatelet in Acute Ischemic Stroke 84  International Stroke Trial (IST)  19,436 patients, ASA 300 mg/day, <48 hors  Chinese Acute Stroke Trial (CAST)  21,106 patients, ASA 160 mg/day, <48 hours  Combined analysis of ASA vs placebo  Absolute risk reduction reduction of deaths or nonfatal stroke: 0.9%  Absolute risk reduction reduction of early stroke recurrence: 0.7%  Small increase in ICH or systemic hemorrhage: IST (1.1% vs 0.6%), CAST (0.8% vs 0.6%) Stroke 2002;33:1934-42
  • 85. Effect of various therapies for treatment of acute ischemic stroke Agent Trial Outcome Effect Aspirin IST Hemorrhagic stroke at 2 wk Harm of 1 per 1000 (NS) Death or nonfatal stroke at 2 wk Benefit of 11 per 1000 (p<0.05) Dead or dependent at 6 mo Benefit of 13 per 1000 (p=0.07) CAST Hemorrhagic stroke at 2 wk Harm of 2 per 1000 (NS) Death or nonfatal stroke at 1 mo Benefit of 7 per 1000 (p=0.03) Dead or dependent at 1 mo Benefit of 11 per 1000 (p=0.08) Heparin IST Recurrent ischemic stroke at 2 wk Benefit of 9 per 1000 (p<0.01) (any dose) Hemorrhagic stroke at 2 wk Harm of 8 per 1000 (p<0.0001) Major extracranial hemorrhage Harm of 9 per 1000 (p<0.0001) Pulmonary embolism Benefit of 3 per 1000 (p<0.05) Death or nonfatal stroke at 2 wk Benefit of 4 per 1000 (NS) Dead or dependent at 6 mo No effect (NS) Heparin IST Recurrent ischemic stroke at 2 wk Benefit of 12 per 1000 (p<0.001) 5000 U bid Hemorrhagic stroke at 2 wk Harm of 3 per 1000 (p<0.05) Major extracranial hemorrhage Harm of 2 per 1000 (NS) Pulmonary embolism Benefit of 12 per 1000 (NS) Death or nonfatal stroke at 2 wk Benefit of 12 per 1000 (p<0.05) Dead or dependent at 6 mo Harm of 2 per 1000 (NS)
  • 86. Antithrombotics for Stroke Prevention 86  Primary stroke prevention  Ischemic stroke prevention  Antiplatelets: aspirin, others  Cardioembolic stroke prevention  Anticoagulants: warfarin, others  Secondary stroke prevention  Ischemic stroke prevention  Antiplatelets: aspirin, dipyridamole, ticlopidine, clopidogrel, glycoprotein IIb/IIIa receptor antagonist  Cardioembolic stroke prevention  Anticoagulants: heparin, warfarin, others
  • 87. Decision-making of antithrombotic therapy for acute ischemic stroke 87 Suspected acute No antithrombotic ischemic stroke Head CT Not completed therapy or reveals ICH Yes Eligible Administer t-PA for t-PA? Aspirin intolerance No or high risk of recurrent stroke Clopidogrel 75 mg/day Head CT ASA 160-300 mg or ASA 25 mg + at 24 hours dipyridamole 200 mg bid Rapid diagnostic evaluation Cardioembolism Large artery Small artery Arterial Cryptogenic atherothrombosis occlusion dissection ASA 100 mg/d Consider anticoagulation Consider ASA, ASA 100 mg/d Consider ASA, Warfarin, INR 2-3 If clopidogrel, or ? anticoagulation no contraindication, Extreme high risk ASA+dipyridamole Consider UFH or ? anticoagulation LMWH

Editor's Notes

  1. General 6) Sodium nitroprusside 另一也同樣屬於 Nitrates 類的藥物, Sodium Nitroprusside ,它的作用機轉和 Nitroglycerin 相似,作用的 onset 及 Duration 都很理想,不過,降壓效果不易控制,需要多次的劑量調整,才能穩定的達到理想血壓,且 Sodium Nitroprusside 會產生有毒的代謝物,除此之外,因其具有光敏感性,所以在使用處理上須避光,並不方便。另外, Sodium Nitroprusside 雖然可以增加冠狀動脈血流,但卻有 Coronary artery steal 的現象,而無法救濟真正缺血的心臟組織。
  2. General 7) Labetalol 這是一個同時具有  及  adrenergic recerptor 的阻斷劑( 7:1 ),因為在降壓的同時並不太會影響到 HR 和 CO ,且血壓控制很穩定,因此不需要進行 Monitor ,在 ICU 中經常使用。可是,其 Onset 太慢, Duration 太長,並不符合理想治療術中高血壓的條件,另外,因其阻斷  及  adrenergic recerptor 故會造成起立性低血壓及尿液滯留,也因為它是  Blocker ,所以也具有一切屬於  Blocker 之禁忌。
  3. General 7) Labetalol 這是一個同時具有  及  adrenergic recerptor 的阻斷劑( 7:1 ),因為在降壓的同時並不太會影響到 HR 和 CO ,且血壓控制很穩定,因此不需要進行 Monitor ,在 ICU 中經常使用。可是,其 Onset 太慢, Duration 太長,並不符合理想治療術中高血壓的條件,另外,因其阻斷  及  adrenergic recerptor 故會造成起立性低血壓及尿液滯留,也因為它是  Blocker ,所以也具有一切屬於  Blocker 之禁忌。