Download 7 stroke part 2

Transient ischemic atack
Clinical picture of TIA
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Neurologic deficits are completelly and
spontaneously reversible in less than 24 hours
– No signs on CT
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TIA is usually characterized by focal neurological
symptoms.
There are 2 main groups of TIA’s symptoms:
– General - usually manifest as headache, dizziness, short
loss of consciousness
– Focal symptoms depend on the vessel territory
TIAs in carotid distribution
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subjective sensory disorders
motor disorders
transient aphasia
blindness or reduction of vision
Focal Jackson motor or sensory epileptic
attacks
TIAs in vertebrobasilar
distribution
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70 % of all TIAs
Vestibular syndrome
Brainstem – cerebellum syndrome
Paresis of oculomotor muscles
Bulbar syndrome
Alternate syndromes
Cortical vision disorders
Atonic – adynamic syndrome - “drop – attacks “
Paroxysmal hypersomnic and katalepsic syndromes
temporal epilepsy
Diagnostic tests in stroke
Diagnosis-Critical Pathway
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Initial
– ECG, Cardiac Enzymes
– Haemogram (blood cell count)
– Coagulation tests – NIR;
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For etiologic diagnosis: genetic conditions - test for C
protein, S protein, factor V, factor VIII, fibrinogen, etc
– Blood proteins; electrophoresis
– glucose, Renal function studies, +/- drug
screen,
Diagnostic Tests
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Noncontrast CT of head
– Differentiate hemorrhage vs ischemia
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MOST ischemic strokes are negative by CT for at least
6 hrs
– Hypodensity indicating infarct seen 24-48 hrs
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Can identify hemorrhage greater than 1cm, and 95%
of SAH
If CT is negative, but still considering SAH may do
lumbar punction
Diagnostic Tests
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Depending on circumstances, other helpful tests
– Echocardiogram – identifies mural thrombus, tumor,
valvular vegetations in suspected cardioembolic stroke
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Transesophagian ecocardiography to see atria
– Echography of arteries in the neck (Doppler, duplex)
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finds out the absence or presence of stenosis and occlusions
of magistral arteries of head and neck.
Dissection
Degree of obstruction of the blood vessel
Type of plaques, risk of emboli formation
Diagnostic Tests
– Angiography – “gold standard” identifies occlusion or
stenosis of large and small vessels of head/neck,
dissections and aneurysms
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Usefull especially in hemorrhage before surgical intervantion
Angio CT, MRA scan – identifies large vessel occlusions –
may replace angiography in the future
– MRI scan – identifies posterior circulation strokes better
and ischemic strokes earlier than CT
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Emergent MRI- considered for suspected brainstem lesion or
dural sinus thrombosis
MRI techniques for recent ischemic stroke: diffusion and
perfusion techniques allow rapid confirmation in vue of
thrombolysis
Treatment of ischaemic
stroke
Ischemic Stroke Management
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General Management
– General support measures
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IV, oxygen, monitor, elevate head of bed slightly
Treat dehydration and hypotension
Avoid overhydration – cerebral edema
Avoid IVF with glucose – except if hypoglycemic
Fever – worsens neurologic deficits
Hypertension
– Treatment indicated for SBP > 220 mm Hg or mean
arterial pressure > 130 mm Hg
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Lowering BP too much reduces perfusion to penumbra
converting reversible injury to infarction
Use easily titratable Rx (labetalol or enalaprilat)
SL Ca-channel blockers should be avoided
Ischaemic stroke treatment –
other management issues
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Surgical:
– Decompression (in selected cases)
– Removal of clot, stenting, I.V. administration of
thrombolitycs
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Brain edema prevention /treatment –
mannitol, loop diuretics (Furosemidum)
Ischaemic stroke - treatment
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Ethiologic
– Trombolysis
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rTPA – tissue plasminogen activator
3 hours from the start of stroke
I.V., generally or directly in the obstructed artery
– Heparin – prevents extension of clot/ formation
of new clots
Thrombolysis Background
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NIH/NINDS study
– 624 patients, trial with I.V. tPA vs placebo
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Treatment w/in 3 hrs of onset
– At 3 months, patients treated with tPA were at least 30%
more likely to have minimal/no disability; absolute
favorable outcome in 11-13 percent
– 6.4% of patients treated with tPA developed symptomatic
ICH compared with 0.6% in placebo group
– Mortality rate at 3 months not significantly different
– tPA group had significantly less disability
– FDA approved in 1996
tPA Dose and Complications
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IV tPA –Total dose 0.9 mg/kg, max. 90mg
– 10% as bolus, remaining infusion over 60 min.
– Blood pressure and Neurological checks every 15
min for 2 hours initially
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Treatment must begin within 4,5 hours
of symptoms and meet inclusion and
exclusion criteria
No ASA or heparin given x 24 hours after
thrombolysis
Thrombolysis Criteria in
Ischemic Stroke
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Inclusion criteria
– Age 18 years or older
– Time since onset well established to be < 3 hrs
– Clinical diagnosis of ischemic stroke
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Exclusion criteria
– Minor/rapidly improving neurologic signs
– Evidence of intracranial hemorrhage on pretreatment
noncontrast head CT
– History of intracranial hemorrhage
– High suspicion of SAH despite normal CT
– GI or GU bleeding within last 21 days
Criteria for IV Thrombolysis – other exclusion criteria
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Exclusion criteria
Known bleeding diathesis
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Platelet count < 100,000 /mm3
Heparin within 48 hours and has an elevated PTT
Current use of anticoagulation or PT > 15 seconds or INR > 1.7
Intracranial surgery, serious head trauma or previous stroke within 3
months
Major surgery within 14 days
Recent arterial puncture at non compressible site
Lumbar puncture within 7 days
Seizure at onset of stroke
History of ICH, AVM or aneurysm
Recent MI
Sustained pretreatment systolic pressure > 185 mmHg or diastolic
pressure > 110 mmHg despite aggressive treatment to reduce BP to
within these limits
Blood glucose < 50 or > 400 mg/dL
Anticoagulants
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Heparin: unproven
– Patients may expect fewer strokes but benefit is
offset by increased ICH
– Similar results with low molecular weight heparin
– Use of heparins or heparinoids for a specific
stroke subtype or TIA cannot be recommended
based on available evidence.
– Prevention of decubitus complications
Drug Therapy in Ischemic Stroke
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Majority of the patients are not thrombolysis
candidates
– secondary prevention
Stroke secondary prevention
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Prevention of risk factors – correct treatment of
diabetes, arterial hypertension, dyslipidemia, giving
up smoking
Antiplatelet agents
– ASA: ↓ risk 20-25% vs placebo
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50-300 mg dose and will not interfere with tPA therapy
– Dipyridamole: alone (200mg BID) ↓ risk 15%
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Dipyridamole + ASA (Assasantin, Aggrenox)
– Clopidogrel: (75 mg qd) 0.5% absolute annual risk reduction
when compared to ASA
– Triflusalum (Aflen)
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Good for pts who cannot tolerate or fail ASA
Stroke secondary prevention
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Anticoagulation - vitamin K antagonists
– warfarine, Acenocumarol
– first line in secondary prevention in patients with
atrial fibrilation or other cardiac emboligene
conditions
– < 75 years – embolic risk – atrial fibrillation
– >75 years (individual evaluation of risk/benefit)
– INR 2.5 (2 –3) lifelong or whole duration of AF
(Vidal, Martindale)
Drug Therapy in Ischemic
Stroke
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Cerebral vasodilators:
– vincamine, vinpocetine, nicergoline,
pentoxifylline
– Ginkgo biloba
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Cerebral trophic agents
– Pyracetam, pramiracetam
– Cerebrolysin, Actovegin
Neuroprotective therapy
Neuroprotective therapy is designed to save the penumbra, or
the area surrounding the core of the primary ischaemia, from
the damage caused by reduced blood flow to this region
Neuroprotection targets
 Growth factors
 Calcium channels
 Glutamate receptors
 Free radicals
 Nitric oxide
 Proteases
 Cell membrane components
 Apoptotic pathway molecules
(e.g. Bcl-2 promoters)
 Neuroprotective drugs:
Cerebrolysin, calcium
blockers
Hemorrhagic stroke
Stroke
Rupture produces
injury by
distorting,
compressing and
tearing the
surrounding brain
tissue or by
increasing
intracranial
pressure
Haemorrhagic
Rupture of a vessel
Intracranial haemorrhage
Anterior
cerebral artery
(ACA)
Circle of Willis
Middle
cerebral
artery
(MCA)
Basilar
artery
Blood in subarachnoid space
Vertebral arteries
Posterior cerebral artery
 Intraparenchymal haemorrhage may be relatively benign
 Bleeding into the region of previous infarction causes no additional functional loss
 At the site of rupture, bleeding into the brain may cause traumatic injury to the exposed
tissue, and blood or its breakdown products in the parenchyma damages brain tissues
Cerebral hemorrhage - etiology
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Arterial hypertension
– Segmentar arteriolosclerosys: fibrinoid necrosis,
hyalinosys, sclerosis of the media: lipohyalinosys
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Small diameter arteries (0,08-0,3 mm)
– Microaneurisms – arteries with 0,3-1 mm diameter
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Damages the intraparenchimal arteries
– Penetrating arteries, near their origin in large arterial
trunks
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(MCA, basilary trunk, superior cerebellar artery, anteroinferior
cerebellar artery)
More frequent location of hemorrhageae within the basal
ganglia, internal capsula, thalamus, pons, cerebellum
Microaneurysms
in penetrating
arteries
Cerebral hemorrhage - etiology
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Vascular malformations
– Arterial aneurysms
– Arteriovenous malformations
– Other small blood vessel malformations (cavernoma,
telangiectasia)
– Micotic aneurysms
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Amyloid angiopathy
– Amyloid deposits in the arterial walls
– All types of intracranial bleeding
– Tendency to recidivate
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Coagulation abnormalities
– Genetic, leucemy
– Anticoagulant treatment
– Drug/alcohol abuse, tumors, systemic diseases, pregnancy,
cerebral venous obstruction
Topographical forms
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Basal ganglia
Lobes
– localized – “intrecerebral
hematoma”
Topographical forms
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Brainstem:
– Primary: pontine
– Secondary:
mesencephalon, in rapid
rising of the intracranial
pressure in tumors,
hemorrhage above the
tentorium
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Cerebellar
– May lead to severe
respiratory problems,
coma, decerebration
– Decompression may be
urgently needed
Brain hemorrhage - treatment
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Prevention:
– Correct treatment of arterial hypertension,
– vessel malformations’ surgical treatment,
– correct monitoring of anticoagulant treatment
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Non surgical:
– General measures of support
– Treatment of seizures, other complications
– Treatment of brain edema – loop diuretics, manitol
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Surgical:
– Bleeding control
– Removal of hematoma
– In lobe hemorrhages, cerebellar hematoma
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Rehabilitation
Subarrachnoid hemorrhage
Causes of SAH
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Rupture of an existing aneurysm
– 85% anteriorly
– Especially the anterior communicating artery
– Aneurysmal size often >7mm and <10mm
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Rupture of an AV malformation
Trauma
Tumour
Distribution of congenital cerebral aneurysms
Arterial aneurysms
Vascular malformations
Subarrachnoid
hemorrhage
•Bleed into the
subarachnoid
space in the brain.
Subarrachnoid hemorrhage
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Clinical picture
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Sudden onset
Intense headache
Vomiting
Meningeal syndrome –
but no fever
– Consciousness
alterations
– Usually no other focal
signs
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Diagnosis
– History
– Non-contrast CT
– May need LP
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If CT is negative or
equivocal
If CT unavailable
Subarrachnoid hemorrhage
Initial Management
 ABC
 Bed rest
 SBP < 160 mm Hg
Complications:
 Early:
– Treat any pain/anxiety
– Hydralazine/SNiP/Others
– May also increase risk of
infarction
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Prevention of seizure
– Load with phenytoin
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Monitor closely for signs of
raised ICP
– Intubated (if not already)
– Hyperventilated
– Mannitol
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– Rebleeding
– Arterial spasm
– Acute hydrocephalus
Surgery (clips/coils/drains)
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Late:
– Recurrence
– Psychiatric sequelae
– Chronical hydrocephalus
Vasospasm
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Occurs 3-30 days after the initial bleeding
Peaks at 4-12 days (worst time for surgery!)
Associated with increased mortality in the first 2
weeks post bleed.
Occurs in 70% of patients presenting with SAH
Diagnosis
– Angiogram or MRA
– Doppler (increased velocity of blood)
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Prevention:
– Hypervolaemic Hypertensive Haemodilution
– Nimodipine
Vasospasm
Venous system
Cerebral venous system
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Superficial system:
– Drains into the venous
synuses
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Central system
– Drain in a large, short
venous trunk – the great
vein of Galien
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Basal system
– Drains the blood into the
basilar vein and then to
the great vein of Galien
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Jugular veins
Cerebral venous trombosys
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Causes:
Infectious – significantly decreased since antibiotics
– Local
– General
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Non infectious
– Local: trauma, surgical interventions, tumors,
arterialtrombosys, malformations
– General: surgicale, pregnancy, post partum/post abortum,
drugs, dehydration, advanced liver or kidney disease
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Idiopatic
Cerebral venous trombosys
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Venous synus thrombosis:
– Increased pressure in the preceding veins (depending on
the anastomosys system)
– increased intracranial pressre
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Superior longitudinal synus: role in resorbtion of the CSF
Cerebral veins thrombosys
– Secondary hemorrhage is more frequent
– Cerebral edema, venous infarcts
– Seizures
Cerebral venous trombosys
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Clinical picture:
– Increased intracranian pressure (headache,
nausea, papillary edema, consciousness
abnormalities)
– Focal or generalized seizures
– Meningean syndrome
– Focal signs
– Septic CVT: fever, other signs of severe infection
Cerebral venous trombosys
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Cavernous synus thrombosys
– Staphilococcus infections of the face, orbitary, synuses,
teeth other ENT infections
– Trauma
– Usually the clinical picture is marked by the septic
syndrome
– Venous stasis:
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Palpebral edema, chemosis, exoftalmia
VI-th and then IIIrd, IV-th, and ophtalmic ramus of the Vth
nerves palsies
– Often clinical signs are bilateral – the 2 synuses are
conected
Cerebral venous trombosys
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Investigations
– CT, MRI
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Thrombus image
Empty vessel (CT with contrast substance)
Infarctus or hemorrhages images
– Arteriography
– CSF analysis – differential diagnosys of an infection
– EEG, funduscopy
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Treatment:
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Etyologic treatment
Antithrombotic treatment (anticoagulants)
Treatment of cerebral edema, raised intracranian pressure,
seizures