STROKE
By
Dr. Bikha Ram Devrajani
FCPS, FACP, FRCP
Professor Medicine
Liaquat University of Medical & Health
Sciences, Jamshoro
BIKHA
Definition of Stroke

Acute focal neurological deficit resulting
from cerebrovascular disease and lasting
more than 24-hours (or causing earlier
death)
BIKHA
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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Haemorrhagic
15%
Ischaemic
85%
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Thromboembolism
Heart
25%
Large Vessels and
others
50%
Small Vessel Disease
25%
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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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Cerebral Infarction
Pathophysiology
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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Pathophysiology
Cerebral 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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Pathophysiology
Cerebral 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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Pathophysiology
Cerebral 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
Free Radical Generation
Mitochondrial Injury
Necrotic Cell Death
Enzyme Activity
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Pathophysiology
Intracerebral 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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Pathophysiology
Intracerebral 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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BIKHA
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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Causes of Intracerebral
Haemorrhage (10-15% of all strokes)
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
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Causes of Intracerebral
Haemorrhage (10-15% of all strokes)
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
BIKHA
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
BIKHA
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
BIKHA
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
BIKHA
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
BIKHA
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
BIKHA
Risk Factors for Cerebral Infarction
R e la tiv e
R is k
E s tim a te d a g e s ta n d a rd is e d p re v a le n c e
o f e x p o s u re in
p o p u la tio n (% )
2 -4
2 -4
2
6
1 -3
3 -1 5
7
30
25
3
1
20
4
2
1 -4
3
D e fin ite
in c re a s in g a g e
m a le g e n d e r
in c re a s in g B P
c ig a re tte s m o k in g
d ia b e te s m e llitu s
a tria l fib rilla tio n
is c h a e m ic h e a rt d is e a s e (IH D )
c a ro tid b ru it/s te n o s is
tra n s ie n t is c h a e m ic a tta c k o r
p re v io u s s tro k e
 p e rip h e ra l v a s c u la r d is e a s e
(in te rm itte n t c la u d ic a tio n )
 in c re a s in g p la s m a fib rin o g en









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Risk Factors for Cerebral Infarction
Possible
 hyperlipidaemia* (definite for IHD)
 hyperhomocystinaemia
 activation of the renin-angiotensinaldosterone 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
BIKHA
Risk Factors for Cerebral Infarction
Possible
 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
BIKHA
Risk Factors for Cerebral Infarction
Possible
 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 eyes
Incontinence of urine or faeces
Confusion
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Non-focal Neurological Symptoms
Any 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
BIKHA
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.
BIKHA
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.
BIKHA
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

BIKHA
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

BIKHA
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

BIKHA
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

BIKHA
The 7 D’s of Stroke Care
Detection:
Dispatch
Delivery
Door
Data
Decision
Drugs
BIKHA
Algorithm for Suspected Stroke:
Goals for Management of Stroke
Identify signs of possible 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
ContinuedBIKHA
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)
ContinuedBIKHA
Does CT scan show any hemorrhage?
No Hemorrhage
Hemorrhage
Probable acute ischemic stroke; consider
Consult neurologist or neurosurgeon;
fibrinolytic therapy:
consider transfer if not available

Check for fibrinolytic exclusions

Repeat neurologic exam: are deficits
rapidly improving to normal
Not a Candidate
Administer aspirin
Patient remains candidate
for fibrinolytic therapy
Candidate

Begin stroke pathway
Review risks / benefits with patient and family: If

Admit to stroke unit if available
acceptable

Monitor BP; treat if indicated

Give tPA

Monitor neurologic status; emergent CT if deterioration

No anticoagulants or antiplatelet treatment for
24 hours

Monitor blood glucose; treat if needed

Initiate supportive therapy; treat comorbidities
BIKHA
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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BIKHA