Stroke – Canadian Stroke Best Practice Guideline 2010

Stroke

  • Sudden onset of neurological deficits (focal, lasting >24hr) of a vascular basis with infarction (permanent tissue injury) of CNS tissue – can be confirmed by neuroimaging
  • Not an evolving neuro deficit over several days
  • Hemorrhagic stroke ~20% & ischemic stroke ~ 80%
Focal arterial Ischemia
  • Pathological imaging / evidence of infarction
TIA
  • Sudden onset of neurological deficits of a vascular basis without infarction (ie. resolution) – reversible, no infarction, no permanent brain injury
  • Up to 20% within 30days (mainly 7 days) go on to develop stroke

CVAs – don’t use this term, not specific

Silent: “subclinical” CNS infarction: imaging or neuropathological evidence of CNS infarction w/o a hx of acute neuro dysfunction attributable to lesion

Ischemic stroke: focal cerebral, spinal, retinal neuro deficit with evidence of tissue damage / lasting > 24hr

Mechanism of stroke:
  • Large vessel: embolic, thrombotic
  • Small vessel: thrombotic
  • Acutely: check CBC, lytes, INR, PTT < liver enzymes, Trop, CXR, EKG
  • Longer: carotid u/s or CTA, lipid profile (LDL), glucose, TTE, 24hr holter
Etiology

20% cariogenic embolism, 25% small vessel dz (lacunar), 20% atherosclerotic CVD, 30% cryptogenic (unknown)


Main Risk factors:
  • Age – risk doubles with every 10 yr after ag 55
  • Aboriginal or black
  • HTN, T2DM, CAD / MI, A Fib
  • abnormal lipid profile
  • Coagulopathy
  • Prior TIA / Stroke
  • Smoking (normal risk after 3-5 yrs of quiting), xs EtOH
  • Centripetal obesity, poor diet, sedentary
  • stress / depression
  • Drugs: OCP, cocaine

1. In patients presenting with symptoms and/or signs suggestive of stroke, include other diagnoses in the differential diagnosis (e.g., transient ischemic attack [TIA], brain tumour, hypoglycemia, subdural hematoma, subarachnoid bleed).

Assessment:
  • Establish Time of onset
  • ABCs, full VS monitoring, check glucose, urgent CODE STROKE if <4.5 h from symptom onset (possible thrombolysis)
  • r/o hemorrhage with CT
  • Consider thrombolysis if no hemorrhage (tPA then no anticoagulation x 24hr)
DDx: Stroke Mimics to r/o:
  • Cerebral:
    • Sz / post-ictal – Todd’s paralysis
    • Mass lesions: Brain tumor, subdural hematoma
  • Anatomic
    • MS
    • Bell’s palsy
      • Peripheral (lower motor neuron) CN VII palsy
      • Corticospinal and corticobulbar tracts
        • Corticobulbar: upper motor neuron usually spares the forehead, vs. lower motor neuron
        • LMN pattern facial palsy → if this is a stroke, they are going to have some cranial neuropathies and weakness on the contralateral side
      • Abrupt onset: unilateral facial paralysis
      • Includes the forehead (central causes will spare the forehead)
      • Tx: steroids and antiviral Tx
    • Mononeuropathy, plexopathy
  • Metabolic:
    • hypoglycemia or other metabolic abnormalities
  • Atypical migraine
  • Somatization / Conversion disorder
  • Vascular:
    • subdural bleed / hematoma, SAH
    • Hypertensive encephalopathy
  • Infectious / inflammatory
    • Abscess, encephalitis
    • Vasculitis
Stroke “chameleons” : relatively rare presentations
  • Limb-shaking TIA
    • Generally alert
    • Fluctuating course, total weakness then jerking mvt
    • Due to 99% occluded carotid, have a few hours before stroke
  • TIAs w/ altered LOC or other brainstem symptoms
    • Generally have cranial neuropathies
    • Ataxia, weakness
  • Spontaneous limb mvts or posturing due to brainstem ischemia
    • High-grade basilar occlusion – decorticate or decerebrate posturing, episodic / recurrent, high-motality
  • Capsular warning syndrome
    • Recurrent high-risk TIA symptoms
      • Happens 2-3 times in 48hr
      • Have a small perforating vessel that is just about to occlude ~5-/50 chance of resolution vs occlusion
Atypical stroke presentation – not often caused by stroke
  1. Amnesia
  2. Obtunded / Coma (unless brainstem stroke)
  3. Confusion (vs Aphasia)
  4. Bilateral symptoms / signs (may be seen with brainstem, but will be associated with cranial neuropathies)
  5. Syncope – generally weakness vs stroke (fall from unilateral weakness)

In office management:
  1. Current symptoms
    • Atypical (gradual onset / spread, Sz, LOC, transient amnesia, isolated vertigo) – consider differential
    • Call 911 if typical symptoms
  2. Symptoms in past 7 days – refer to stroke clinic to be seen in 24 hrs or ER
  3. Symptoms >7d ago
    • Refer to stroke clinic to be seen in 1 mo
    • Do investigations & secondary management

2  In a patient presenting with a stroke, differentiate, if possible, hemorrhagic from embolic/thrombotic stroke (e.g., through the history, physical examination, and ancillary testing, such as scanning and electrocardiography), as treatment differs.

S/Sx:Hemorrhagic
  • ↑ ICP – H/A, N/V, Sz
  • Meningismus
  • ↓ LOC, focal deficits / motor weakness
  • blown pupil, hx of trauma
Ischemic
  • Nystagmus, Visual field defect / neglect, diplopia, amaurosis fugax
  • Facial pain / numbness, ipsilateral tongue weakness, slurred speech
  • Dysarthria, dysphagia
  • Ataxia, limb/truncal weakness, hemiparesis
  • Inattention, impulsivity – silent stroke often missed

Approach to Dx:
  • Age and other demographic data
    • Is there a high % of a cerebrovascular event?
  • Nature of the symptoms: Stroke causes negative symptoms generally
    • Positive: xs CNS electrical discharges: visual (flashing lights etc), somatosensory (pain, paresthesia), motor (jerking mvts)
    • Negative: loss of reduction of CNS function (loss of vision / hearing / sensation / power)
  • Onset and progression
    • Symptoms tend to be abrupt and maximal at onset (vs evolving over minutes – hrs)
  • Duration
  • Precipitating factors: stress, EtOH, position change
  • Associated symptoms: H/A, LOC, during or after attacks?

Case: Unable to speak, slumped over, unable to move right hand / leg

  • Likely dominant hemisphere, given evidence of Broca’s involvement
Hx:
  • Need to know time of onset – was there a definite time, when last seen and speak normally
    • unknown onset time if woke up with a headache
  • Are they improving?
  • Do FAST?
  • Get them a scan?
PE:
  • Check ABCs/ IV/Monitor/ BG
  • FACE – sens 82%, spec 37% (score 1 point for each of three)
    • Face: smile – is there drooping of one side?
    • Arm: check for drift downward when raising arm?
    • Speech: ask to repeat simple phrase – slurred or strange?
 Ix:

Acute:

  1. Non-contrast CT head STAT to r/o hemmorhage & assess extent of infarct (infarcts often don’t show up until 24-48 hr)
    • 26% sensitivity in detection of early ischemia
    • We do these acutely to r/o haemorrhage and tumour.
    • Signs of stroke
      • Loss of cortical white-grey differentiation
      • Sulcal effacement: mass effect decreases visualization of sulci
      • Hypodensity of parenchyma
      • Insular ribbon sign
      • Hyperdense MCA sign
    • Standardized approach to looking at stroke CT in acute phase: ASPECT score, for prognostic information
      • Score out of 10, loose one point for greying out or edema in certain areas
    • LP if suspected SAH
  2. ECG to r/o A fib
  3. Echo to r/o cardioembolic cause (with bubble studies to r/o PFO)
  4. CBC, electrolytes, renal function, PTT/INR, blood glucose

Not Acute Ix:

  1. Holter / Echo
  2. Lipids, FBG, TSH
    • Consider ESR, VDRL, APLA, Factor V, Protien C/S
  3. Carotid U/S (? stenosis)
  4. MRI scan = 83% sensitivity in acute phase (ischemic changes appear within hours)
  5. Cerebral angiography – gold standard

3  Assess patients presenting with neurologic deficits in a timely fashion, to determine their eligibility for thrombolysis.

Thrombolysis – rtPA (recombinant tissue plasminogen activator)
  • Given within 4.5 h of acute ischemic stroke onset provided there are clinical indications and no c/i to use
    • If they are over 80yrs, we don’t generally give tPA because the trails excluded those with severe stroke and age over 80yrs
    • Prognosis: age, severity of stroke syndrome and age
    • <2% receive tPA (because we are not great at diagnosing stroke, we’re slow and so most patient’s not lysed
    • Punumbra: With every stroke, there is the infarcted core and surrounding tissue at risk (thepunumbra) → this is why they will get worse with time if not urgently treated
      • For every minute you save to tPA, it’s a day of rehab
  • Indications – NIH stroke scale (NIHSS) to determine the severity of an acute stroke and monitor response to Tx over time
    • rtPA should be considered if NIHSS ≥ 6
    • 11 items that evaluate:
      • LOC,
      • Visual system,
      • motor system,
      • sensory system,
      • language abilities
    • 0 = no stroke, 1-4 = mild, 5-15 = moderate, 15-20 = moderate to severe, 21-42 = severe stroke
  • Absolute C/I:
    • Hx:
      • improving sx, minor sx, Sz at stroke onset,
      • recent major Surgery (within 14 d) or trauma, recent GI or urinary hemorrhage (21d),
      • recent LP or arterial puncture at noncompressible site
    • PMH:
      • ICH, Sx of SAH /
      • pericarditis / MI,
      • pregnancy
    • PE:
      • sBP ≥ 185, dBP ≥ 110, aggressive Tx to ↓ BP,
      • uncontrolled serum glucose,
      • thrombocytopenia
    • Ix:
      • hemorrhage or mass on cT,
      • high INR or aPTT

4  In a patient diagnosed with stroke, involve other professionals as needed (e.g., a physical therapist, an occupational therapist, social service personnel, a physiatrist, a neurologist) to ensure the best outcome for the patient.

Stroke Rehabilitation
  • May require inpatient program & continuation through home care or outpatient services
Multidisciplinary approach:
  • dysphagia assessment & dietary modifications,
  • communication rehabilitation,
  • cognitive & psychological assessments – screen for depression,
  • therapeutic exercise programs,
  • assessment of ambulation & evaluation of need for assistive devices, splints or braces,
  • vocational rehabilitation

5  When caring for a stroke patient with severe/serious deficits, involve the patient and her or his family in decisions about intervention (e.g., resuscitation, use of a feeding tube, treatment of pneumonia).


6  In patients who have suffered stroke, diagnose “silent” cognitive deficits (not associated with sensory or motor symptoms or signs, such as inattention and impulsivity) when they are present.


7  Provide realistic prognostic advice about their disabilities to stroke patients and their families.

Lacunar (subcortical) stroke –small vessel, prognosis and w/u is different than cortical

  • generally lacunar are from DM and HTN, not generally cardiac origin
  • Most common: Pure motor hemiparesis (face, arm, leg equal weakness w/out sensory deficits or aphasia)
  • Pure sensory loss (equal involvement of the face, arm, leg, trunk)
  • Generally lacunar are of sudden onset, once in a while they have a stuttering course

Cortical signs: (these are not seen with lacunar strokes)

  • Dominant hemisphere, aphasia, field cut, sensory loss
  • Non-dominant: field cut, neglect, face and arm>leg weakness

 8  In stroke patients with disabilities, evaluate the resources and supports needed to improve function (e.g., a cane, a walker, home care).


9  In the continuing care of stroke patients with deficits (e.g., dysphagia, being bedridden), include the prevention of certain complications (e.g., aspiration pneumonia, decubitus ulcer) in the treatment plan, as they are more common.

Stroke complications in the acute phase:
  • DVTs – DVT prophylaxis if bed-bound
  • delirium,
  • infections (aspiration pneumonia, UTIs)
  • Dysphagia – NPO if dysphagia (to be reassessed by SLP)
  • depression (up to 50%),
  • bedridden & sacral ulcer – padding, change of positions
  • post-stroke pain, etc…
    • All of these will set patients back neurologically
    • DVT prophylaxis if no evidence of haemorrhage on CT
  • Initiate rehabilitation early
  • Silent cognitive deficit: inattention, impulsivity

10  In patients at risk of stroke, treat modifiable risk factors (e.g., atrial fibrillation, diabetes, hyperlipidemia, and hypertension).

Lifestyle: – for both 1o and 2o preventions
  • Healthy diet: ≥ 5 servings of fruit / vegi or Mediterranean diet (vegetarian, fats high on olive/canola oil, low trans fat)
  • Moderate exercise: 5d/wk – 150min / week
  • Smoking cessation
  • BMI 18.5-24.9
  • EtOH limit <2/d for male and <1/d for female
Risk factors Modification: 90% recurrent TIA/stroke can be prevent, greatest risk in 1st wk post TIA
1/5 will have subsequent stroke / MI or die within one year
Carotid Stenosis
  1. Primary Prevention (Asymptomatic)
    • Carotid endarterectomy is controversial: if stenosis >60%, risk of stroke 2% /yr. – carotid endarterectomy reduces the risk by 1%/yr but 5% risk of complications
    • Tx with ASA + carotid endartectomy if stenosis >50% + symptomatic or >60%(per guiedline)
    • No screening!
  2. Secondary Prevention (previous stroke / TIA in carotid territory)
    • All pt should have carotid u/s within 24 hr of stroke
    • Carotid endarterectomy benefits those with symptomatic severe stenosis (70-99%) & is less beneficial for those with symptomatic moderate stenosis (50-69%) – NASCET trial
    • Early risk of stroke after TIA in patient with internal carotid artery disease
      • Transient Retinal ischemia or brain ischemia (hemispheric, amaurosis fugax) → consider carotid endarectomy
      • In younger patients, may consider stenting, but not favoured generally because may not be as durable in the long-term (older patients have more tortuous brittle arteries – do not do well with stent, so even though they generally have higher peri-op risk they overall do better with endarectomy)
A Fib – 1° & 2° prevention
  • CHADS2 score
    • 0 = antiplatelet
    • 1 = anticoagulant or antiplatelet – pt specific decision (CHADSVASC)
    • >2 = anticoagulant
      • Warfarin – INR 2-3 (if valvular A fib)
      • Dabigatran 100 / 150mg bid (in preference to warfarin CCS2014 guideline)
      • Don’t need anti-plt
  • Strokes fromAFib (cardioembolic)tendtobeworse, because more clot burden and tend to bleed more (vs.arterioembolic from carotids)
    • When you’re looking for AFib with large vessel event, ~2-3% tends to be picked up on 24h holter à tend to need prolonged external loop recorder (15% of the time you’ll pick up AFib)
    • Can prevent recurrent stroke by 90% if you detect and anti-coagulate w/ AFib
HTN
  • 1°: BP <140/90 or 130/80for diabetics and renal dz – tx per HTN guidelines
    • Ramipril 10mg po od (HOPE trial) – ACEI reduce the risk of stroke beyond their antihypertensive effect
  • 2°: ACEI & thiazide are recommended in pt with previous stroke / TIA (PROGRESS trial)ACEI & thiazide are recommended in pt with previous stroke / TIA (PROGRESS trial)
    • for each 10mmHg, reduce risk by 1/3 → aggressive HTN control
  •  Medication non-compliance: 50% of patients are not taking meds at 6mos post stroke clinic
Hypercholesterolemia
  • 1°: Statin ↓ stroke risk in CAD pt or high CV events pt, even with normal cholesterol (CARE trial)
  • 2°: Statin ↓ risk of subsequent stroke – high dose atorvastatin (SPARCL trial)
  • Monitor Q1-3 yr, ↑ frequency if abnormal – Target LDL <2 or 50%↓
Diabetes
  • A1C <7% & fasting BG 4-7, post-prandial 5-10
  • ASA 81-325mg in all pt with DM + CVA
Smoking
  • Dose-dependent ↑ stroke risk
  • After smoking cessation, the risk of stroke decreases to baseline within 2-5 yr
OSA
  • Screen pt post stroke
  • Avoid sedative, use positional Tx, wt loss, CPAP, dental appliances

11  In all patients with a history of TIA or completed stroke, and in asymptomatic patients at high risk for stroke, offer antithrombotic treatment (e.g., acetylsalicylic acid, clopidogrel) to appropriate patients to lower stroke risk.

ABCD2 Score – predict / identify pt at high risk of stroke following TIA
0-3 = low (urgent f/u)
4-5 = moderate (Admission and observation)
6-7 = high risk (admission & w/u & initiation of Tx)
  • Age > 60yo: 1
  • BP >140/90: 1
  • Clinical Features:
    • 2 – unilateral weakness,
    • 1 – speech disturbance w/o focal weakness
  • Duration of symptoms:
    • 1 – 10-59min,
    • 2 – >60min
  • Diabetes: 1

Anti-platelet therapy

Primary prevention
  • NO evidence for low-risk pt w/o a prior stroke / TIA
Secondary prevention
  • ASA is the initial antiplatelet of choice for stroke prevention:
  • ACEi if BP >130
  • Holter / carotid u/s
  • High risk TIA: short-termtx for risk reduction – CHANCE study (Chinese)
    • Day 1: load w/ Plavix 300mg + ASA 650mg
    • Day 2-21: Plavix 75mg + ASA 81
    • Day 22-90: Plavix 75mg, no ASA
    • Afterwards,
      • if ASA naïve consider revert to ASA 81 long-term
      • if was on ASA prior, consider Plavix 75 indefinitely without ASA
    • Note in elderly patients may shorten the double antiplatelet interval to less than 3-weeks especially if lots of white matter disease, atrophy, etc…
  • Other agents reserved for those suffer cerebrovascular symptoms while on ASA or unable to tolerate ASA
    • Aggrenox (ESPRIT trial)
    • Clopidogrel (CAPRIE trial)
  • Patients w/ lacunar stroke:
    • Prolonged double anti-platelet therapy for more than 10-14 days probably more risk than benefit, so tend to shorten the double antiplatelet period, then continue either ASA or Plavix indefinitely
  • No benefit & increase risk of bleeding to combining ASA + clopidogrel (MATCH & CHARISMA trials)

Stroke syndromes:
  1. Embolic: rapid onset, sx max at onset
  2. Thrombotic: progression of sx over hr to days possibly with stuttering course
ICA/Ophth:
  • Amaurosis fugax (transient monocular blindness)
ACA:
  • Hemiplegia (leg > arm)
  • Confusion, abulia, urinary incontinence, primitive reflexes
MCA
  • Hemiplegia (arm & face > leg)
  • Hemianesthesia, homonymous hemianopia
  • Aphasia if dom. hemisphere: sup. div → expressive; inf → receptive
    • 95% of Right handed have language on left side
    • 60% of Left handed have language on left side
  • Apraxia and neglect if nondominant hemisphere
  • Drowsiness & stupor seen later (due to brain swelling)
PCA
  • Thalamic syndromes with contralateral hemisensory disturbance, aphasia
  • macular-sparing homonymous hemianopia
Vertebral
  • Wallenberg syndrome = numbness of ipsilateral face and contralateral limbs
  • diplopia, dysarthria, ipsilateral Horner’s
Basilar
  • Pinpoint pupils
  • Long tract signs: quadriplegia and sensory loss
  • CN abnormalities & cerebellar dysfunction
Lacunar
  • Pure hemiplegia, pure hemianesthesia
  • ataxic hemiparesis or dysarthria + clumsy hand

Reference:
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Posted in 88 Stroke, 99 Priority Topics, FM 99 priority topics, Neuro

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