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STROKE
By
Dr. Bikha Ram DevrajaniFCPS, FACP, FRCP
Professor MedicineLiaquat University of Medical & Health
Sciences, Jamshoro
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Definition of Stroke
Acute focal neurological deficit resulting from cerebrovascular disease and lasting more than 24-hours (or causing earlier death)
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Definition of Stroke
Stroke is not a diagnosis but a clinical syndrome with numerous causes
The main types of stroke and their relative occurrence are:
Cerebral infarction (85%) Intracerebral haemorrhage (10%) Subarachnoid haemorrhage (5%)
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Transient Ischaemic Attack (TIA)
Also defined as an acute focal neurological deficit resulting from cerebrovascular disease, but the symptoms and signs resolve within 24-hours
Most patients recover within 30-min No fundamental difference between TIA and
stroke except for the duration of the symptoms
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Epidemiology of Stroke Stroke is the third leading cause of death in
the United States and a leading cause of serious, long-term disability.
In the United States there is one stroke patient in every 45 seconds.
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Ischaemic85%
Haemorrhagic15%
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Large Vessels and others50%
Small Vessel Disease25%
Thromboembolism Heart25%
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Pathophysiology
Clinical Classification of Focal Stroke. Transient if the deficit recover within 24 h. Completed if the focal deficit is persistent. Evolving if focal deficit continues to worsen
after about 6 h from onset.
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Pathophysiology
Cerebral Infarction Infarction is a process which takes some
hours to complete.
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Pathophysiology
Cerebral Infarction
a. Occlusion of a cerebral artery, the opening of anastomatic channels from other arterial territories may restore perfusion.
b. Reduction in perfusion pressure leads to homeostatic changes to maintain oxygenation of brain vasodilation of cerebral artery.
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PathophysiologyCerebral Infarction
c. If homeostatic process fails ischaemia begins - ultimately leads to infarction.i. When the blood-flow falls below threshold for
maintenance of electrical activity neurological deficit appears – but neurons are still viable. At this stage if blood-flow restores then recovery will be definite (TIA).
ii. If flow further falls, then cell death process starts.
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Pathophysiology
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PathophysiologyCerebral Infarction
Final result of occlusion of a cerebral blood vessel depends upon:
i. Competence of the circulatory homeostatic mechanism.
ii. Severity of reduction of blood-flow.
iii. Duration of reduction of blood-flow.
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Pathophysiology
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PathophysiologyCerebral Infarction If ischaemic damage is affecting the
endothelium of vessel then there is chance of haemorrhage in the infarction by blood’s thrombolytic mechanism.
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PathophysiologyCerebral Infarction Radiologically infarct can be seen as a
lesion which is composed of:• Ischaemic.
• Swollen but recoverable (pnemubra).
• Finally infarcted area will be replaced fluid filled cavity (liquification necrosis).
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Ischaemia
Energy Failure
Depolarization
Glutamate Release
Na+/Ca++ Influx
Cellular Swelling
Mitochondrial Injury
Free Radical Generation
Enzyme Activity
Necrotic Cell DeathNecrotic Cell DeathNecrotic Cell DeathNecrotic Cell Death
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PathophysiologyIntracerebral Haemorrhage Cessation of functions of affected parts. As neurons are structurally distrupted and
white matter fibre tract split apart. Rim of cerebral oedema around
haemorrhage.
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PathophysiologyIntracerebral Haemorrhage If big haemorrhage the shifting of midline
and transtentorial causing rapid death. If survives then haemosidrin lined slit in
brain parenchyma.
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CT Scan of Intracerebral Haemorrhage
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Causes of Cerebral Infarction(75-80% of all strokes)
Large artery atherothromboembolism =50%• Extracranial (aorta, carotid, vertebral arteries)
= 40-45%
• Intracranial (ICA, MCA, ACA, vertebral, basilar, PCA) = 5-10%
Small artery diseases (microatheroma/lipohyalinosis) = 20-25%
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Causes of Cerebral Infarction(75-80% of all strokes)
Large artery atherothromboembolism =50%• Extracranial (aorta, carotid, vertebral arteries)
= 40-45%
• Intracranial (ICA, MCA, ACA, vertebral, basilar, PCA) = 5-10%
Small artery diseases (microatheroma/lipohyalinosis) = 20-25%
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Causes of Cerebral Infarction(75-80% of all strokes) Contd:
Embolism from the heart = 20% Non-atheromatous arterial disease (e.g.
dissection, arteritis) = 5% Blood disease (thrombophilia) <5%
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Cardiac Sources of Embolism(in anatomical sequence)
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Cardiac Sources of Embolism(in anatomical sequence)
Right to left shunt (paradoxical emboli from the venous system) via:
Patent foramen ovale Atrial septal defect Ventricular septal defect Pulmonary arteriovenous malformation
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Cardiac Sources of Embolism(in anatomical sequence) Contd.
Left Atrium Thrombus:
• atrial fibrillation*• sinoatrial disease (sick sinus syndrome)• atrial septal aneurysm
Myxoma and other tumours*
* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd:
Mitral Valve Rheumatic endocarditis (stenosis* or
regurgitation) infective endocarditis* Mitral annulus calcification Mitral valve prolapse
* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd:
Mitral Valve Non-bacterial thrombotic (marantic)
endocarditis. Libman-Sacks endocarditis Prosthetic heart valve*
* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd:
Left Ventricle Mural thrombus:
• acute myocardial infarction (within previous few weeks)*
• left ventricular aneurysm or akinetic segment
• dilated cardiomyopathy*
* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd:
Left Ventricle Mural thrombus:
• mechanical ‘artificial’ heart*• blunt chest injury (myocardial contusion)
Myxoma and other tumours*
* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd:
Aortic Valve Rheumatic endocarditis (stenosis or
regurgitation). Infective endocarditis* Syphilis Non-infective thrombotic (marantic)
endocarditis* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd:
Aortic Valve Libman-Sacks endocarditis Prosthetic heart valve* Calcific stenosis/sclerosis/calcification
* substantial risk of embolism
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Cardiac Sources of Embolism(in anatomical sequence) Contd.
Congenital heart disease (particularly with right to left shunt)
Cardiac manipulation/ surgery/ catheterisation/ valvuloplasty/ angioplasty
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
A. Arterial Disease (anatomical factors) ‘Complex’ disease (fibrinoid necrosis) in
small, penetrating vessels:• most common cause in middle and old age
hypertensives• haemorrhages often deep in putamen (40%),
caudate nucleus (85%), thalamus (15%), cerebral hemispheres (lobar) (20%), cerebellum (8%), and brainstem (8%)
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
A. Arterial Disease (anatomical factors) Amyloid (congophilic) angiopathy*
• most common cause in old age• haemorrhages often in lobes of cerebral
hemispheres• may be associated with dementia
* causes of multiple haemorrhages in the brain parenchyma
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A. Arterial Disease (anatomical factors) Vascular malformations (arteriovenous
and cavernous angiomas)• dural or brain• most common cause of ICH in young
normotensive people• seizures and headaches commonly antedate
haemorrhage• cavernous angiomas tend to be multiple and
familial
Causes of Intracerebral Haemorrhage (10-15% of all strokes)
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A. Arterial Disease (anatomical factors) Caroticocavernous fistula Hereditary haemorrhagic telangiectasia Saccular aneurysms
• cause 1 in 13 intracerebral haemorrhages (2 in 13 <65 years old), usually in conjunction with subarachnoid haemorrhage
Causes of Intracerebral Haemorrhage (10-15% of all strokes)
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
A. Arterial Disease (anatomical factors) Atheromatous aneurysm Septic arteritis and mycotic aneurysms Necrotising angitis of the CNS* Arterial dissection
* causes of multiple haemorrhages in the brain parenchyma
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
A. Arterial Disease (anatomical factors) Intracerebral tumours
• primary (glioblastoma, oligodendroglioma, medulloblastoma, haemangioblastoma)
• metastases (melanoma, bronchial carcinoma, renal carcinoma, choriocarcinoma, endometrial carcinoma)
Intracranial venous thrombosis*
* causes of multiple haemorrhages in the brain parenchyma
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
A. Arterial Disease (anatomical factors) Moyamoya syndrome Occult head injury* Trauma Haemorrhagic brain infarction
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
B. Raised Blood Pressure (haemodynamic factors)
Acute arterial hypertension Alcohol (also antiplatelet action, and
coexistent liver disease) Amphetamines (may also cause a
vasculitis) Cocaine and other sympathomimetic drugs
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
B. Raised Blood Pressure (haemodynamic factors)
Monoamine oxidase A inhibitors Exposure to extreme cold Trigeminal nerve stimulation Post carotic endarterectomy, heart
transplantation, or correction of congenital heart lesions
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
B. Raised Blood Pressure (haemodynamic factors)
Chronic arterial hypertension, causing complex small vessel disease (see above)
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
C. Bleeding Diathesis (haemostatic factors)*
Anticoagulants• risk of intracerebral haemorrhage is about
1% per year• Increased risk if elderly, previous stroke,
hypertensive, small vessel disease, and if INR > 4.0
* causes of multiple haemorrhages in the brain parenchyma
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
C. Bleeding Diathesis (haemostatic factors)*
Antiplatelet drugs: probably a relatively minor contributory factor
Thrombolytic treatment• 0.75% of patients with myocardial infarction
(>2% risk if elderly >65 years, low body weight <70-kg, hypertensive, and given alteplase as opposed to streptokinase; 0.3% risk if none of these risk factors)
* causes of multiple haemorrhages in the brain parenchyma
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Causes of Intracerebral Haemorrhage (10-15% of all strokes)
C. Bleeding Diathesis (haemostatic factors)*
Thrombocytopenia Haemophilia & other hereditary
coagulation factor deficiencies (e.g. factor V) Leukaemia Diffuse intravascular coagulation
* causes of multiple haemorrhages in the brain parenchyma
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Risk Factors for Cerebral InfarctionRelative
RiskEstimated age-
standardised prevalenceof exposure inpopulation (%)
Definite increasing age male gender increasing BP 2-4 30 cigarette smoking 2-4 25 diabetes mellitus 2 3 atrial fibrillation 6 1 ischaemic heart disease (IHD) 1-3 20 carotid bruit/stenosis 3-15 4 transient ischaemic attack or
previous stroke7 2
peripheral vascular disease(intermittent claudication)
1-4 3
increasing plasma fibrinogen
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Risk Factors for Cerebral InfarctionPossible
hyperlipidaemia* (definite for IHD) hyperhomocystinaemia activation of the renin-angiotensin-
aldosterone system high plasma factor VII coagulant activity low blood fibrinolytic activity raised haematocrit
* probable weak (or under-researched) positive association with ischaemic stroke, and possible weak inverse/negative association
with haemorrhagic stroke
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Risk Factors for Cerebral InfarctionPossible
raised von-Willebrand factor antigen raised tissue plasminogen activity antigen plasma viscosity (largely determined by
plasma fibrinogen) physical inactivity obesity snoring and sleep apnoea
* probable weak (or under-researched) positive association with ischaemic stroke, and possible weak inverse/negative association
with haemorrhagic stroke
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Risk Factors for Cerebral InfarctionPossible
recent infection family history of stroke diet (salt, fat) alcohol (none, or heavy drinking) race social deprivation stress
* probable weak (or under-researched) positive association with ischaemic stroke, and possible weak inverse/negative association
with haemorrhagic stroke
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Infarction
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Infarction
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Haemorrhage
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Focal Neurological and Ocular Symptoms
Motor Symptoms weakness or clumsiness of one side of
the body, in whole or in part (hemiparesis) simultaneous bilateral weakness
(paraparesis, quadriparesis)* difficulty swallowing (dysphagia)* imbalance (ataxia)*
* as an isolated symptom, this does not necessarily indicate focal brain ischaemia or haemorrhage because there are many other
potential causes
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Focal Neurological and Ocular Symptoms
Speech/Language Disturbances difficulty understanding or expressing
spoken language (dysphasia) difficulty reading (dyslexia) or writing
(dysgraphia) difficulty calculating (dyscalculia) slurred speech (dysarthria)*
* as an isolated symptom, this does not necessarily indicate focal brain ischaemia or haemorrhage because there are many other
potential causes
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Focal Neurological and Ocular Symptoms
Sensory Symptoms Somatosensory
• altered feeling on one side of the body, in whole or in part (hemisensory disturbance)
* as an isolated symptom, this does not necessarily indicate focal brain ischaemia or haemorrhage because there are many other
potential causes
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Focal Neurological and Ocular Symptoms
Sensory Symptoms Visual
• loss of vision in one eye, in whole or in part (monocular blindness)
• loss of vision in the left or the right half or quarter of the visual field (hemianopia, quadrantanopia)
• bilateral blindness• double vision (diplopia)*
* as an isolated symptom, this does not necessarily indicate focal brain ischaemia or haemorrhage because there are many other
potential causes
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Focal Neurological and Ocular Symptoms
Vestibular Symptoms a spinning sensation (vertigo)*
Behavioural/Cognitive Symptoms difficulty dressing, combing hair, cleaning
teeth etc.; geographical disorientation; difficulty copying diagrams such as a clock, flower, or intersecting cubes (visual-spatial-perceptual dysfunction)
forgetfulness (amnesia)** as an isolated symptom, this does not necessarily indicate focal
brain ischaemia or haemorrhage because there are many other potential causes
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Non-focal Neurological Symptoms
Generalised weakness and/or sensory disturbance‘Blackouts’ with altered or loss of consciousness or fainting, with or without impaired vision in both eyesIncontinence of urine or faecesConfusion
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Non-focal Neurological SymptomsAny of the following symptoms, if isolated:*
A spinning sensation (vertigo) Ringing in ears (tinnitus) Difficulty swallowing (dysphagia) Slurred speech (dysarthria) Double vision (diplopia) Loss of balance (ataxia)
* If these symptoms occur in combination, or with focal neurological symptoms, they may indicate focal cerebral ischaemia
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DIFFERENTIAL DIAGNOSIS OF ISCHEMIC STROKE & TIA
Clinical diagnosis of ischemic or hemorrhagic stroke depends upon clinicians understanding of brain function and pathology.
Deficit that evolve over weeks are usually caused by:• Brain mass either primary or metastatic
brain tumor.• Brain abscess.• Sub-dural hematoma.
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DIFFERENTIAL DIAGNOSIS OF ISCHEMIC STROKE & TIA
TIA may be confused with classic or
complicated:
• Migraine.
• Seizures.
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DIFFERENTIAL DIAGNOSIS OF ISCHEMIC STROKE & TIA
Hemorrhagic stroke often enters in
differential diagnosis:
• Ischemic strokes.
• Verterobasillary ischemia.
• Non-specific dizziness.
• Meinier’s disease.
• Peripheral vestibulopathy.
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Differential Diagnosis of Stroke (in order of frequency of occurrence in general practice)
Metabolic/toxic encephalopathy (hypoglycaemia, non-ketotic hyperglycaemia, hyponatraemia, Wernicke-Korsakoff syndrome, hepatic encephalopathy, alcohol and drug intoxication)
Functional/non-neurological (e.g. hysteria) Epileptic seizure (postictal Todd’s paresis)
or non-convulsive seizures
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Elements of Patient Management within a Specialist Stroke Unit
Standardised (protocol driven) investigation and management
Risk assessment for swallowing Active treatment of contributory factors Early rehabilitation Multidisciplinary team Rationalise medication Research opportunities Discharge planning
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Tips on Triples in Acute Stroke: Some Points Worth Remembering
3 h window for safe and effective thrombolysis
Avoid thrombolyis if infarction already affects more than 1/3 of MCA territory
Control blood sugar tightly for 3 days Start blood pressure treatment after 3
days Take decision on tube feeding at 3 days
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Tips on Triples in Acute Stroke: Some Points Worth Remembering
Three complications to avoid: aspiration, venous thrombosis, infection
Three groups of patients (atherothrombotic, cardioembolic and haemorrhagic) get three different treatment: aspirin, warfarin or neither
Delay warfarin for 3 weeks after significant embolic infarct
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The 7 D’s of Stroke Care
Detection: Dispatch Delivery Door DataDecision Drugs
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Algorithm for Suspected Stroke:Goals for Management of Stroke
Critical EMS assessments and actions : Support ABCs; give oxygen if needed Perform prehospital stroke assessment Establish time when patient last known normal (Note: therapies
may be available beyond 3 hours from onset) Transport; consider triage to a center with a stroke unit if
appropriate; consider bringing a witness, family member or caregiver
Alert hospital Check glucose if possible
Identify signs of possible stroke
Continued
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Immediate general assessment and stabilization: Assess ABCs, vital signs Provide oxygen if hypoxemic Obtain IV access and blood samples Check glucose; treat if indicated Perform neurologic screening assessment Activate stroke team Order emergent CT scan of brain Obtain 12-lead ECG
Immediate neurologic assessment by stroke team or designee Review patient history Establish symptom onset Perform neurologic examination (NIH Stroke Scale or Canadian
Neurologic scale)
Continued
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Does CT scan show any hemorrhage?
Probable acute ischemic stroke; consider
fibrinolytic therapy:
Check for fibrinolytic exclusions Repeat neurologic exam: are deficits
rapidly improving to normal
Consult neurologist or neurosurgeon;
consider transfer if not available
HemorrhageNo Hemorrhage
Patient remains candidate for fibrinolytic therapy
Administer aspirin
Not a Candidate
Begin stroke pathway Admit to stroke unit if available Monitor BP; treat if indicated Monitor neurologic status; emergent CT if
deterioration Monitor blood glucose; treat if needed Initiate supportive therapy; treat comorbidities
Review risks / benefits with patient and family: If
acceptable Give tPA No anticoagulants or antiplatelet treatment for
24 hours
Candidate
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Critical Time Periods
Immediate general assessment 10 minutes
Immediate neurologic assessment 25 minutes
Acquisition of head CT 25 minutes
Interpretation of the CT Scan 45 minutes
Administration of fibrinolytics, timed from ED arrival 60 minutes
Administration of fibrinolytics, timed from onset of symptoms 3 hours
Admission to a monitored bed 3 hours
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