1
Guidelines for Management of
Stroke
Ulaanbaatar 2012
2
Contents
Abbreviations 4
Introduction 5
А. General Part 6-8
А.1. Definition of Stroke
А.2. International Classification Disease Codes
А.3. Users of this Guideline
А.4. Objective
А.5. Processed Data
А.6. Update Data
А.7. Participants in preparing this guideline
А.8. Used terminology
A.9. Epidemiology
B. Management of Ischemic Stroke 8-20
B.1. Assessment and management of acute stroke
B.1.1. Orders and steps of emergency medical services
B.1.2. Referral and patient transfer
B.1.3. Emergency room management of Acute Stroke
B.1.4. Diagnosis of Stroke
B.1.5. Treatment decisions by stroke team
B.1.6. Treatment for Ischemic Stroke
B.1.6.1. General stroke treatment
B.1.6.2. Specific treatment
B.1.6.3. Thrombolytic therapy
B.1.6.4. Management for Hypertension
B.1.6.4.1. Management of hypertension in patients eligible or not eligible for
thrombolytic therapy
B.1.6.5. Antiplatelet and anticoagulant therapy
3
D. Management of Spontaneous Intracerebral Hemorrhage 20-26
C.1. Diagnosis of Intracerebral hemorrhage
C.2. Treatment of acute Intracerebral hemorrhage
C.2.1. Air way and oxygenation
C.2.2. Medical treatment
C.2.3. Blood pressure management
C.2.4. Surgical removal of Intracerebral hemorrhage
D. Management of Aneurysmal Subarachnoid Hemorrhage 26-30
D.1. Manifestations and diagnosis of aneurysmal SAH
D.2. Medical management of SAH
D.3. Surgical and endovascular treatment of ruptured cerebral aneurysms
D.4. Medical measures to prevent re-bleeding after SAH
D.5. Management of cerebral vasospasm
E. Management of complications in Strokes 31-34
E.1. Therapy of elevated Intracranial pressure and Hydrocephalus
E.1.1. Management of intracranial pressure
E.2. Prevention and management of other complications in Strokes
F. Rehabilitation 34-35
H. Prevention of Stroke 35-39
H.1. Primary prevention
H.2. Secondary prevention
I. Application of the guidelines for management of stroke
in each level of medical organizations 40
References 41
4
Abbreviations
AF atrial fibrillation
BP blood pressure
CAS carotid artery stenting
CEA carotid endarterectomy
CE-MRA contrast-enhanced MR angiography
CSF cerebral spinal fluid
CT computed tomography
CTA computed tomography angiography
CV cardiovascular
DSA digital subtraction angiography
DWI diffusion-weighted imaging
ECG electrocardiography
ED emergency department
EEG electroencephalography
EMS emergency medical service
FLAIR fluid attenuated inversion recovery
ICA internal carotid artery
ICP intracranial pressure
INR
ICH
international normalized ratio
Intracerebral hemorrhage
iv
IS
intravenous
Ischemic stroke
LDL low density lipoprotein
MCA middle cerebral artery
MI myocardial infarction
MRA magnetic resonance angiography
MRI magnetic resonance imaging
mRS modified Rankin score
NASCET North American Symptomatic Carotid Endarterectomy Trial
NIHSS National Institutes of Health Stroke Scale
NINDS National Institute of Neurological Disorders and Stroke
OSA obstructive sleep apnoea
PE pulmonary embolism
PFO patent foramen ovale
pUK pro-urokinase
QTc heart rate corrected QT interval
RCT randomized clinical trial
rtPA recombinant tissue plasminogen activator
SAH Subarachnoid hemorrhage
TCD transcranial Doppler
TOE transoesophageal echocardiography
TIA transient ischemic attack
TTE transthoracic echocardiography
UFH unfractionated heparin
5
Introduction
Stroke is one of the leading causes of morbidity and mortality worldwide. WHO statistics indicate
that all types of stroke ranked cause of death (13-15%) as the third and surpassed only by heart
disease and cancer. Each year 15.000.000 persons suffer from stroke worldwide out of which
5.000.000 and up with mortality and the remaining 10.000.000 have been deeply disabled. Each
year, Mongolia registered 270-290 cases of stroke in 100.000 populations ,thereby belonging to
countries with higher incidence of stroke.
Many advances have been made in stroke prevention, treatment, and rehabilitation. For
example, thrombolytic therapy can limit the extent of neurologic damage from stroke and
improve outcome, but the time available for treatment is limited. Healthcare providers, hospitals,
and communities must develop systems to increase the efficiency and effectiveness of stroke
care. The “7 D’s of Stroke Care”— detection, dispatch, delivery, door (arrival and urgent triage in
the emergency department [ED]), data, decision, and drug administration — highlight the major
steps in diagnosis and treatment and the key points at which delays can occur.
The goal of stroke care is to minimize brain injury and maximize patient recovery. The
community-oriented “Stroke Chain of Survival” that links actions to be taken by patients, family
members, and healthcare providers to maximize stroke recovery are the following:
– Rapid recognition and reaction to stroke warning signs;
– Rapid emergency medical services (EMS) dispatch;
– Rapid EMS system transport and hospital pre-notification;
– Rapid diagnosis and treatment in the hospital;
– Rehabilitation;
– Primary prevention;
– Secondary prevention;
The guidelines summarize the management of 3 types of acute strokes: (1) Ischemic Stroke and
Transient Ischemic Attack; (2) Intracerebral Hemorrhages; and (3) Aneurysmal Subarachnoid
Hemorrhage in the adult patients.
The guidelines for management of strokes developed by leading experts of Mongolia were
approved by the Council of Neurology at Ministry of Health Mongolia and recommended to
introduce into out-of-hospital and ED assessment and In-hospital stroke management.
6
A. General
A1. Definition of Stroke
Stroke is an acute focal neurological deficit caused by a vascular lesion; The onset is sudden
and the symptoms last longer than 24 hours, if the patient survives.
Ischemic stroke is an acute focal neurological deficit caused by a vascular occlusive lesion with
sudden onset and symptoms lasting longer than 24 hours.
Transient ischemic attack is a neurological deficit lasting less than 24 hours, with complete
clinical recovery, caused by focal hypoperfusion within the brain.
Intracerebral hemorrhage is an acute focal neurological deficit caused by rupture of
microaneurysms secondary to chronic hypertension.
Subarachnoid hemorrhage is a spontaneous arterial bleeding into the subarachnoid space,
caused by rupture of arterial aneurysm or AVM.
А.2. International Classification of Disease codes (ICD-10)
I63-I67: Cerebral Infarction
G45-G46: Transient Ischemic attack
I61-I67.9: Intracerebral Hemorrhage
I60-I60.9: Subarachnoid Hemorrhage
A.3. Users of this Guideline
The guidelines would be used by personnel of Emergency Aid, Stroke Units, Neurological Clinics
and Neurosurgery and Rehabilitation specialists.
A.4. Objective
These guidelines are directed to emergency room personnel sand stroke specialists for
management of acute ischemic stroke, TIAs, Intracerebral and subarachnoid hemorrhages and
their prevention in the modern era.
A.5. Processed Date: From June to September 2011
A.6. Update Date: 2016
A.7. Participants for preparing this guideline:
G.Tsagaankhuu
A.Kuruvilla
Consultant Neurologist, Department of Neurology, Health
Sciences University
WHO consultant
J.Ariunaa Chairman, Neurological Center, State Third Central Hospital
J.Sarangerel Director, Reflex Hospital
R.Amarbayasgalan
G.Baigalmaa
U.Saraa
Head of Neurological clinic, State First Central Hospital
Neurologist, State Third Central Hospital
Neurologist, State Third Central Hospital
Ts.Delgermaa Neurologist, State First Central Hospital
Ts.Ouyngerel Neurologist, State First Central Hospital
L.Enkhsaikhan Neurologist, State First Central Hospital
7
O.Tsetsgee Anesthesiologist, State Third Central Hospital
D.Enkhbold Neurosurgeon, State Third Central Hospital
R.Munkhbayar Neurologist, Reflex Hospital
D.Baasanjav Medical Research Institute, President of Mongolian Neurology
Association
D.Ulziibayar Department of Neurology, HSUM
L.Otgonbayar Head, Department of Neurology, HSUM
Ts.Burmaa Standardization and Measurement Agency
N.Ouynbileg Millennium Challenge Account Mongolia, Project of Health
personnel
S.R.Govind
D.Narantuya
PMO/Team Leader HSD, NCD, MCH, ENH WHO Mongolia
WHO, Project of “Stroke and Heart Infarction”
Review and confirmation of guidelines:
Organizations Responsible for completion
Meeting for guidelines developing working
groups under MOH; from Aug, 2011 to
Nov,2012 (6 times)
Meeting of Mongolian Neurology Association’s
governors 27th Aug,2011
Chief, Working group J.Ariunaa
President of Mongolian Neurology Association
D.Baasanjav
MOH, Board of Neurology; 16thFebruary, 2012 MOH, Board of Neurology; G.Tsagaankhuu
HSUM, Council of terminology; 17th February,
2012
HSUM, Council of terminology;
G.Tsagaankhuu
MOH, Health medical aid and standardization
technical committee;
Meeting of MOH governor 15th Nov,2012
MOH, Government Implementation Agency –
Department of Health; Ts.Khun
MOH, State secretary for Health
J.Khatanbaatar
A.8. Used terminology:
– Aneurysm
– Ischemic stroke or cerebral Infarction
– Transient ischemic attack
– Reversible ischemic neurologic deficit (RIND)
– Progressing cerebral infarction
– Thrombus infarct
– Cardiogenic infarct
– Lacunar Infarct
– Hemodynamic infarct
– Intracerebralhemorrhage
– Subarachnoid hemorrhage
– Antithrombotic therapy
– Thrombolysis
– Stroke unit
– Carotid endarterectomy
– Angioplasty
– Stent
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A.9. Epidemiology
In the Western industrialized countries age-adjusted stroke incidence rates range between 100-
300 per 100.000 people per year. Every year, in the United States about 700.000 people of all
ages suffer a new or repeat stroke. Approximately 158.000 of these people will die, making
stroke the third leading cause of death in the United States. Each year, Mongolia registered 270-
290 cases of stroke in 100.000 populations, thereby indicating that Mongolia has high rate of
stroke incidence as compared with average stroke incidence rates in the world. In the developed
countries, cerebral infarction accounted for 87% of all stroke types. In Mongolia, the ratio of brain
infarction versus intracerebral hemorrhage is 1:1 thereby showing that adequate control of
hypertension and preventive measures against stroke are not optimal in Mongolia.
Epidemiological studies suggest that ischemic strokes account for 80-85%, hemorrhagic strokes
for 15-20% and subarachnoid hemorrhages for 10%. Of ischemic strokes, cardioembolism
account for 15-30%, atherosclerotic infarction accounts for 15-40%.
B. Management of Ischemic Stroke (Cerebral Infarction)
Cerebral ischemia is caused by blockage vascular supply in the local region of the brain, except
during the general circulatory failure due to cardiac arrest and systemic hypotension. Occlusion
of the cerebral artery typically results in an area (the “core”) so severely ischemic that will be
damaged irreversibly within minutes or hours, surrounded by a less ischemic penumbra of
neuronal tissue that may be temporarily inactivated. In fact, the ischemic penumbra can be
defined as a severely ischemic area, functionally impaired; consisting of potentially surviving
brain tissue that is at risk of infarction, but that can recover if it is reperfused in time. If the
occluded artery reopens early and sufficiently with subsequent improvement or normalization of
the blood supply, the ischemic lesion will be small or absent and its clinical expression might well
be a TIA.
The three leading causes of cerebral infarcts are:
• Extra- and intracranial large artery disease
• Cardioembolism
• Small artery disease (microangiopathy)
About one-third of the sources of stroke remain undiagnosed even if carefully investigated.
Atherosclerotic large artery disease is the presumed cause of cerebral infarcts in 15-40% of
patients. The principal sites of atherosclerotic plaque are in the internal carotid artery at the
extracranial bifurcation, carotid siphon, and large intracranial arteries (more often seen in Asians
and Black African Americans).
In the posterior circulation similar lesions occur in the proximal and distal vertebral arteries, and
in the basilar artery.
Ischemic stroke is also classified into subgroups based on the postulated mechanisms of
infarction and duration of progressing ischemia:
• Embolic stroke occurs when thrombus from heart (cardioembolic stroke) or another
blood vessel (artery-to artery embolism) breaks and occludes more distal cerebral artery.
• Lacunar infarct or small vessel disease develops when focal atherosclerotic lesion
leads to occlusion of penetrating artery deep in the brain parenchyma.
• Hemodynamic infarct is considered to be hemodynamic when there is evidence of flow
failure. Mostly, this may involve the boarder-zone of cerebral arteries and caused by
severe stenosis or occlusion of a large artery (ICA or VA).
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• Transient ischemic attack (TIA) is defined as temporary episode of focal ischemic
neurologic dysfunction that completely resolves within 24 hours.
• Reversible ischemic neurologic deficit (RIND) or a minor stroke is considered when
focal ischemic deficit persists for longer than 24 hours but resolves within 3 weeks.
• Cerebral infarctions(Ischemic strokes) is characterized by persisting of focal
neurologic deficits longer than 3 weeks.
• Progressing cerebral infarction is considered when rapid evolution of ischemic
cerebral vascular events occurs in patients who have increasing neurologic deficit for as
long as 72 hours after the onset symptoms. This stroke syndrome is more common in the
territory of vertebrobasilar system.
Defined diagnosis of stroke and the differentiation between ischemic and hemorrhagic stroke
cannot be made on clinical grounds alone. Specific treatments can be initiated only after the
diagnosis of an ischemic or hemorrhagic stroke has been established with an adequate
radiological examination.
10
Goals for management of patients with suspected stroke algorithm
1
2
Time goals
33
3
4
5 5
7
6
8 9
10 11
Recognition of stroke symptoms
Emergency medical service:
– Support ABC; give oxygen if needed by nasal cannula
– Perform pre-hospital assessment of stroke
– Establish time when patient last known normal(Note: thrombolysis
therapy available within 3 hours from onset!)
– Transport to a hospital with stroke unit;take a witness and caregiver
– Notification to the receiving hospital
– Check blood sugar if possible
Arrival to Emergency
department: 10min
Immediate general assessment and stabilization:
– Assess ABC and vital signs
– provide oxygen if hypoxemic
– Obtain IV access
– Obtain blood samples
– Check blood sugar, treat if needed
– Perform neurologic screening assessment
– Activate stroke team
– Order Immediate brain CT scan
– Obtain 12-lead ECG After arrival to
Emergency
department: 25min
Immediate neurological assessment by stroke team or specialist of stroke:
– Review patient history
– Establish symptomsonset
– Perform neurologic examination and assess by the NIHSS
After arrival to
Emergency
department: 45min
Does CT scan show any Hemorrhage?
Consult neurologist or neurosurgeon;
consider transfer if not available
No hemorrhage Hemorrhage
Possible acute ischemic stroke: consider iv thrombolysis
therapy
– Establishcontraindications
– Repeat neurologic exam: are symptoms rapidly reduced to
normal?
Not a
candidate
Patient remains candidate for
thrombolysis?
Administer aspirin
After arrival to
Emergency
department: 60min Candidate
– Start general stroke treatment
– Admit to stroke unit if available
– Monitor BP; treat if indicated
– Monitor neurologic status; emergent CT if
deterioration
– Check blood sugar; treat if needed
– Start supportive therapy
– Treat comorbidities
Review with patient and family about
the superiority and risk:
– Give rt-PA
– No anticoagulants or antiplatelet for 24
hours
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B.1. Assessment and management of acute stroke
Any patient suspected of having a stroke should be transported as quickly and safely as
possible to the nearest hospital with staff experienced in acute stroke management and
emergency brain imaging. The emergency aid to the stroke patients can be taken in a
short time in following orders:
• Pre-hospital recognition stroke symptoms;
• Transportation to the hospital with stroke unit;
• Assessment of general condition and neurological status of patients in stroke unit;
• Immediate clinical and neuroimaging diagnosis;
• Immediate starting of general and specific appropriate treatment;
B.1.1. Orders and steps of emergency medical services
Step 1: Identify signs of a possible stroke
Step 2: Call 103 immediately (activate EMS system)
This is an important step because EMS responders can transport the patient to a hospital that
provides acute stroke care and notify the hospital that the patient is coming. The hospital staff
can then prepare for efficient Assessment and management of the patient. Currently, half of all
stroke victims are driven to the ED by family members or friends.
B.1.2. Referral and patient transfer
Step 3. Emergency medical service assessments and actions
Table 1. EMS personnel assessments and actions
Assessments Actions
Define and recognize the signs of stroke Support the ABCs (airway, breathing,
and circulation)
Assess the patient using the “Face-Arm-Speech Test” Give oxygen as needed
Establish time zero
Time Zero: set the time when the
patient was last known to be
neurologically normal. If the patient
was sleeping and wakes up with
symptoms, time zero is the last time
the patient was seen to be normal
Consider triage at a stroke center, if possible Transport the patient quickly.
Assess neurologic status while the patient is being
transported
Bring a family member or witness to
confirm time zero
Alert the receiving hospital
Check glucose levels
12
Table 2. Prehospital stroke Scale (Cincinnati criteria)
Facial Droop (have patient show teeth or smile):
• Normal—both sides of face move equally
• Abnormal—one side of face does not move as well as the other side
Arm Drift (patient closes eyes and holds both arms straight out for 10 seconds):
• Normal—both arms move the same or both arms do not move at all (other findings, such as
pronator drift, may be helpful)
• Abnormal—one arm does not move or one arm drifts down compared with the other
Abnormal Speech
• Normal—patient uses correct words with no slurring
• Abnormal—patient slurs words, uses the wrong words, or is unable to speak
Interpretation: If any 1 of these 3 signs is abnormal, the probability of a stroke is 72%.
Table 3. Prehospital stroke Scale (Los Angeles criteria)
Criteria Yes Unknown No
1. Age >45 years □ □ □
2. History of seizures or epilepsy □ □ □
3. Symptom duration <24 hours □ □ □
4. At baseline, patient is not wheelchair
bound or bedridden
□ □ □
5. Blood glucose between 60 and 400 □ □ □
6. Obvious asymmetry (right vs left) in any
of the following 3 exam categories
(must be unilateral):
□ □ □
Equal R Weak L Weak
Facial smile/grimace □ □ Droop □ Droop
Grip □ Weak grip
□ No grip
□ Weak grip
□ No grip
□ Weak grip
□ No grip
Arm strength □ □ Drifts down
□ Falls rapidly
□ Drifts down
□ Falls rapidly
Los Angeles criteria sensitivity 93%, specificity 97%
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B.1.3. Emergency management in the Emergency Department (ED)
Time goal: 10 min
Step 4: Within 10 minutes of the patient’s arrival in the ED, take the following actions
Table 4. Stroke unit services
Actions
Assess ABCs and evaluate vital signs.
Give oxygen if patient is hypoxemic (less than 92% saturation). Consider oxygen if patient is not
hypoxemic.
Make sure that an IV has been established.
Take blood samples for blood count, coagulation studies, and blood glucose. Check the patient’s
blood glucose and treat if indicated. Give dextrose if the patient is hypoglycemic. Give insulin if
the patient’s serum glucose is more than 300. Give thiamine if the patient is an alcoholic or
malnourished.
Assess the patient using a neurologic screening assessment, such as the NIH Stroke Scale
(NIHSS).
Order a CT brain scan and have it read quickly by a qualified specialist.
Obtain a 12-lead ECG and assess for arrhythmias.
Do not delay the CT scan to obtain the ECG. The ECG is taken to identify a recent or ongoing
acute MI or arrhythmia (such as atrial fibrillation) as a cause of embolic stroke. Life-threatening
arrhythmias can happen with or follow a stroke.
B.1.4. Diagnosisof stroke
Time goal: 25 min
Step 5. Within 25 minutes of the patient’s arrival, take the following actions:
Table 5. Stroke team actions
Actions
Review the patient’s history, including past medical history.
Perform a physical exam.
Establish time zero, if not already done.
Perform a neurological exam to assess patient’s status using the NIHSS.
The CT scan should be completed within 25 minutes from the patient’s arrival in the ED
and should be read within 45 minutes; Establish neurological and CT diagnosis
14
Table 6. Emergency diagnostic tests in acute stroke patients
In all patients
1 Brain Imaging: CT or MRI
2 ECG
3 Laboratory Tests: Complete blood count and platelet count, prothrombin time or INR,
Partial Thrombin Time (PTT) Serum electrolytes, blood glucose, C-reactive protein
(CRP) or sedimentation rate, Hepatic and renal chemical analysis
When Indicated
4 Extracranial and transcranial Duplex / Doppler ultrasound
5 MRA or CTA
6 Diffusion and perfusion MR or perfusion CT
7 Echocardiography (transthoracic and/or transoesophageal)
8 Chest X-ray
9 Pulse oxymetry and arterial blood gas analysis
10 Lumbar puncture
11 EEG
Table 7. Recommended requirements for centers managing acute stroke patients
Primary stroke center Comprehensive stroke center
Availability of 24-hour CT scanning MRI / MRA / CTA
Established stroke treatment guidelines and
operational procedures, including intravenous rtPA protocols
Transoesophageal echocardiography
Close co-operation of neurologists,
internists and rehabilitation experts
Cerebral angiography
Specially trained nursing personnel Transcranial Doppler sonography
Early multidisciplinary stroke unit rehabilitation including speech therapy, occupational therapy and physical therapy
Extracranial and intracranial colour-coded
duplex sonography
Neurosonological investigations within 24
hours (extracranial Doppler sonography)
Specialized neuroradiological,
neurosurgical and vascular surgical
consultation (including telemedicine
networks)
Transthoracic echocardiography Carotid surgery
Laboratory examinations (including
coagulation parameters)
Angioplasty and stenting
15
Monitoring of blood pressure, ECG, oxygen
saturation, blood glucose, body temperature
Automated monitoring of pulse oxymetry,
blood pressure
Automated ECG monitoring at bedside Established network of rehabilitation
facilities to provide a continuous process of
care, including collaboration with outside
rehabilitation center
Table 8. National Institutes of Health Stroke Scale (NIHSS)
Stroke scale
Assess level of consciousness
Alert
Drowsy
Stuporous
Coma
0
1
2
3
Movement of legs:
(elevate both legs to30° for 5 seconds)
а) left
b) right
No drift
Drift
Some effort against gravity
No effort against gravity
No movement
0
1
2
3
4
sAssess orientation (month, age)
Both correct
One correct
Two incorrect
0
1
2
Coordination of limb
Normal
One arm or one leg no coordination
Two limb no coordination
0
1
2
Follow commands
(1) Open & close eyes; (2) make fist & release)
Obeys both correctly
Obeys one correctly
Two incorrect
0
1
2
Sensory
Normal
Partial loss
Dense loss
0
1
2
Follow finger (gaze)
Normal
Partial gaze palsy
Forced deviation
0
1
2
Language (аphasia)
Normal
Mild to moderate aphasia
Severe aphasia
Mute/ Complete -Global aphasia
0
1
2
3
Visual field
Normal
Partial hemianopia
Complete hemianopia
Bilateral loss
0
1
2
3
Speech clarity
Normal articulation
Mild to moderate slurring
Nearly unintelligible, mute
0
1
2
Facial palsy
Normal
Minor asymmetry
Partial
Complete
0
1
2
3
Inattention
No neglect
Partial neglect
Profound neglect
0
1
2
Movement of arms:
(elevate both arms to90°for full 10 seconds)
а) left
b) right
No drift
Drift
Some effort against gravity
No effort against gravity
No movement
0
1
2
3
4 Total
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B.1.5. Treatment decisions by stroke team
Time goal: 45 min
Step 6. Within 45 minutes of the patient’s arrival, the specialist must decide, based on the CT scan or
MRI, if a hemorrhage is present.
Table 9. Stroke unit specialist actions
Take these actions if a hemorrhage is present Take these actions if a hemorrhage is
NOT present
Note that the patient is not a candidate for
thrombolytics.
Decide if the patient is a candidate for
thrombolytic therapy.
Arrange for a consultation with a neurologist or
neurosurgeon.
Review criteria for IV thrombolytic therapy by
using the thrombolytic checklist
Consider transfer, if available. Repeat the neurologic exam (NIHSS)
If the patient is rapidly improving and moving to normal, thrombolytics may not be necessary.
B.1.6. Treatment of Ischemic Stroke
B.1.6.1. General stroke treatment
The term “general treatment” refers to treatment strategies aimed at stabilizing the critically
ill patient in order to control systemic problems that may impair stroke recovery; the
management of such problems is a central part of stroke treatment. General treatment
includes respiratory and cardiac care, fluid and metabolic management, blood pressure
control, the prevention and treatment of conditions such as seizures, venous
thromboembolism, dysphagia, aspiration pneumonia, other infections, or pressure
ulceration, and occasionally management of elevated intracranial pressure. It is common
practice to actively manage neurological status and vital physiological functions such as
blood pressure, pulse, oxygen saturation, blood glucose and temperature. Neurological
status can be monitored using validated neurological scales such as the NIH Stroke Scale
or the Scandinavian Stroke Scale. There is little direct evidence from randomized clinical
trials to indicate how intensively monitoring should be carried out, but in stroke unit trials it
was a common practice to have a minimum of 4-hourly observations for the first 72 hours
after stroke. Close monitoring is also required for the first 24 hours after thrombolysis. More
invasive monitoring procedures, such as central venous catheters or intracranial pressure
monitoring, are used only in highly selected patient groups.
General principles of caring for patients with Ischemic stroke
1. Provide ongoing monitoring of neurologic status (level of consciousness, focal deficit, GCS);
2. Establish cardiac monitoring;
3. Airway and oxygenation; Oxygen should be administered if the oxygen saturation falls
below 95%;
17
4. Elevate head of bed 30 degrees;
5. Routine blood pressure lowering is not recommended following acute stroke; Cautious
blood pressure lowering is recommended in patients with extremely high blood
pressures (>220/120 mmHg) on repeated measurements, or with severe cardiac failure,
aortic dissection, or hypertensive encephalopathy;
6. It is recommended that low blood pressure secondary to hypovolemia or associated with
neurological deterioration in acute stroke should be treated with volume expanders;
7. Provide enteral nutrition with nasogastric tube for patients with decreased level of
consciousness or impaired gag reflex;
8. Maintain normovolemia and normal sodium level by starting with administration of 2-3
liters/day solutions of 0.9 normal saline;
9. Treat increased ICP as needed;
10. Monitoring serum glucose levels is recommended;Treat if serum glucose levels >180
mg/dl (>10mmol/l) with insulin titration; Severe hypoglycaemia (<50 mg/dl [<2.8mmol/l])
should be treated with intravenous dextrose or infusion of 10–20% glucose;
11. Give therapy directed at specific aspects of stroke pathogenesis (recanalization of
vessel occlusion or prevention of mechanisms leading to expansion the infarct size).
12. No maintenance dextrose / lactate drip should be given in acute stroke. Only normal
saline infusions should be given as maintenance infusion.
B.1.6.2. Specific treatment
Time goal: 60 min (from onset of stroke symptoms)
If the patient is a candidate for thrombolytic therapy (recombinant tissue plasminogen activator),
review the risks and benefits of therapy with the patient and family (the main complication of IV tPA is
intracranial hemorrhage) and give the tissue plasminogen activator.
Do not give anticoagulants or antiplatelet treatment for 24 hours after tPA until a follow-up CT scan at
24 hrs does not show intracranial hemorrhage.
If the patient is NOT a candidate for thrombolytic therapy, give the patient aspirin.
For both groups (those treated with tPA and those given aspirin), give the following basic stroke care:
Begin stroke pathway
Support patient’s airway, breathing, and circulation
Check blood glucose
Watch for complications of stroke and fibrinolytic therapy
Transfer patient to intensive care if indicated
Patients with acute ischemic stroke who are hypoglycemic tend to have worse clinical outcomes, but
there is no direct evidence that active glucose control improves outcomes. Consider giving IV or
subcutaneous insulin to patients whose serum glucose levels are greater than 10 mmol/L (about 200
mg/dL).
18
B.1.6.2.1. Thrombolytic therapy
Use the thrombolyticchecklist to screen candidates for thrombolytictherapy.
Table 10. Thrombolytic Checklist
Inclusion criteria Exclusion criteria Exclusion criteria
Age: 18 yrs or older Evidence of intracranial
hemorrhage from CT scan
Active internal bleeding or acute
trauma, such as a fracture
Diagnosis of an
ischemic stroke with
neurologic deficit
Clinical presentation suggestive
of a subarachnoid hemorrhage,
even with normal CT
Acute bleeding diathesis, including the
following but may include other
manifestations:
• Platelet count < 100,000/mm3
• Heparin received within 48 hours
prior to onset of stroke, with elevated
activated partial thromboplastin time
(aPTT)
• Current use of anticoagulant (e.g.,
warfarin) with an elevated
international normalized ratio (INR)
> 1.7
Time from onset of
symptoms is within 3
hours
Evidence of multilobar infarction
in more than one-third of the
cerebral hemisphere on CT
Intraspinal surgery, serious head
trauma, or previous stroke within the
past 3 months
History of intracranial
hemorrhage
Arterial puncture at a non- compressible
site within the past 7 days
Uncontrolled hypertension based
on repeated measurements of
>185 mm Hg systolic pressure or
> 110 mm Hg diastolic pressure
Known AV malformation,
neoplasm, or aneurysm
Witnessed seizure at stroke
onset
Relative Contraindications/Precautions
Minor or rapidly improving stroke symptoms
Major surgery or serious trauma within the past 14 days
Recent gastrointestinal or urinary tract hemorrhage within the past 3 weeks
Post-myocardial infarction pericarditis
Recent acute myocardial infarction within the past 3 months
Abnormal blood sugar level < 50 mg/dl or > 400 mg/dl
19
Complications. The major complication of IV tPA is intracranial hemorrhage. Other bleeding
complications, ranging from minor to severe, may also happen. Angioderma and transient
hypotension also can occur.
Research. Several studies have shown that good to excellent outcomes are more likely when tPA is
given to adults with acute ischemic stroke within 3 hrs of onset of symptoms. However, these results
happened when tPA was given in hospitals with a stroke protocol that adheres closely to the
therapeutic regimen and eligibility requirements of the NINDS protocol. Evidence from prospective
randomized studies in adults documented a greater likelihood of benefit when early treatment is
started.
Table 11. Intravenous infusion recombinant tissue plasminogen activator (rt-PA) in
patients with an acute Ischemic stroke
Intravenous infusion of rt-PA
• Alteplase (actilyse) 0.9 mg/kg, with 10% of the dose given as a bolus followed by
a60 min infusion, maximum dose is 90 mg;
• Patient should be admitted to stroke unit or emergency department with a skilled
care facility and close observation unit;
• Neurological examination should be repeated during rt-PA infusion in every15
min, following 6hrs in each 30 min, and next 24hrs in every 1 h
• If patient’s condition worsens during infusion of rt-PA, the infusion should be
discontinued and send for rapid brain CT scan to detect possible bleeding;
• Frequent checking of BP: after starting infusion for 2hrs in each 15 min, following
6hrs in each 30 min, next 24hrs in each 1 h
• Other precautions see table 10
• CT scan to detect possible bleeding for any patient with neurological worsening
after administration of rt-PA;
• Management life-threatening hemorrhagic complications by (1) discontinuing
ongoing infusion of rt-PA, (2) obtaining blood samples for coagulation testing, (3)
obtaining surgical consultation as needed and (4) implementation of other
interventions that may be useful (plasma transfusion, fibrinogen cryoprecipitate
(6-8 units), platelets concentrate (6-8 units);
B.1.6.3. Management for Hypertension
B.1.6.3.1. Managing Hypertension in patients eligible or not eligible for thrombolytic
therapy (tPA)
For patients who are candidates for thrombolytic therapy, control their blood pressure to lower their
risk of intracerebral hemorrhage following administration of tPA.
20
Table 12. Candidates eligible for thrombolytic therapy
PRETREATMENT
Systolic > 185 or diastolic > 110 Labetalol 10 to 20 mg IV for 1–2 min—may repeat 1 time or
nitropaste 1–2 inches
During or after TREATMENT Check blood pressure every 15 min for 2 hrs, then every 30
min for 6 hrs, and finally every hr for 16 hrs
Monitor blood pressure Check blood pressure every 15 min for 2 hrs, then every 30
min for 6 hrs, and finally every hr for 16 hrs
Diastolic > 140 Sodium nitroprusside 0.5 µg/kg per minute IV infusion as
initial dose and titrate to desired blood pressure
Systolic > 230 or diastolic 121 to 140
Labetalol 10 mg IV for 1–2 min—may repeat or double every
10 min to maximum dose of 300 mg or give initial labetalol
dose and then start labetalol drip at 2 to 8 mg/min
OR
Nicardipine 5 mg/hr IV infusion as initial dose and titrate to
desired effect by increasing 2.5 mg/hr every 5 min to
maximum of 15 mg/hr; if blood pressure is not controlled by
nicardipine, consider sodium nitroprusside
Systolic 180 to 230 or diastolic 105
to 120
Labetalol 10 mg IV for 1–2 min—may repeat or double every
10 to 20 min to a maximum dose of 300 mg or give initial
labetalol dose, then start labetalol drip at 2 to 8 mg/min
Table 13. Candidates NOT eligible for thrombolytic therapy
Blood pressure level, mm Hg Treatment
Systolic ≤220 or diastolic ≤120
Observe patient unless there is other end-organ
involvement.
Treat the patient’s other symptoms of stroke (headache,
pain, nausea, etc).
Treat other acute complications of stroke, including
hypoxia, increased intracranial pressure, seizures, or
hypoglycemia.
Systolic > 220 or diastolic 121 to 140
Labetalol 10 to 20 mg IV for 1–2 min—may repeat or
double every 10 min to a maximum dose of 300 mg
OR
Nicardipine 5 mg/hr IV infusion as initial dose; titrate to
desired effect by increasing 2.5 mg/hr every 5 min to max
of 15 mg/hr
Aim for a 10% to 15% reduction in blood pressure
Diastolic > 140 Nitroprusside 0.5 µg/kg per min IV infusion as initial dose
with continuous blood pressure monitoring
Aim for a 10% to 15% reduction in blood pressure
21
B.1.6.4. Antiplatelet and anticoagulant therapy
1. Aspirin (81-325 mg/day, commonly 325 mg)
• Initial treatment low grade stenosis in anterior or posterior circulation
• Initial treatment in symptomatic high grade stenosis intracranial carotid artery,
vertebrobasilar system, or extracranial carotid artery, if not candidate for warfarin or
operation
• Initial treatment in selected patients with transient ischemic attack (TIA) or minor stroke
(nonsurgical candidate in anterior circulation ischemia)
2. Clopidogrel (75 mg/day)
• Recurrent symptoms in spite of aspirin therapy /aspirin failure, contraindication to warfarin
in setting of high grade arterial stenosis (nonsurgical candidate in anterior circulation
ischemia) or cardiac source emboli
• Initial treatment in selected patients with transient ischemic attack (TIA) or minor stroke
(nonsurgical candidate in anterior circulation ischemia)
• Allergic or sensitive to aspirin, requiring antiplatelet therapy
3. Warfarin anticoagulation (INR 2.0-3.0), short-term (3 months), followed by antiplatelet agent
• Symptomatic low grade stenosis anterior and posterior circulation
• Symptomatic occlusion of carotid, vertebral, or basilar artery with associated
thromboembolic symptoms (use warfarin 4-6 wk or 3 months, INR 2.0-3.0)
• Symptomatic high grade stenosis in intracranial carotid artery, vertebrobasilar system, or
extracranial carotid artery, if not a surgical candidate
• Cardiac source of emboli, level and duration of anticoagulation depending on cause
4. Heparin anticoagulation
• Intravenous infusion in appropriate patients with cerebral infarction may be initiated with a
bolus of 5000 U followed by constant infusion of 800-1000 U/h under the control of
activated partial thromboplastin time (aPTT) with the normal control value 1.5-2.0 times –
should be monitored every 6 hours until the therapeutic value has been documented and
then daily during the time of infusion (hemorrhagic complications 1-7% in large ischemic
stroke)
• Treatment sometimes includes low-molecular-weight heparins (flaxiparine, calciparine),
which have less side effects for causing complications than usual unfractionated heparin.
• Low dose Enoxaparin (Lovenox) 30 mg sc daily for deep vein thrombosis prophylaxis
among seriously ill patients.
C. Management of Spontaneous Intracerebral Hemorrhage (ICH)
Intracerebral hemorrhage occurs when the hemorrhage penetrates into the parenchyma of the
brain and it most commonly caused by arterial hypertension and subsequent small vessel
disease and amyloid angiopathy (primary ICH) or by vascular malformation (secondary ICH).
The clinical signs of ICH range from asymptomatic bleeding to sudden death. Immediate stages
are:
• Mild to severe head ache
• Focal neurologic deficits
• Global cerebral deficits, ranging from mild disturbance of consciousness to coma
The pattern of clinical signs and secondary complications reflect the neurotopology and size of
the ICH (hematoma in the cortex, subcortex, brain stem and cerebellum, or intraventricular
22
hemorrhages) and indicate prognosis. Clinically, ICH cannot be distinguished from cerebral
ischemia, although some clues suggest one possibility more than the other. For example, ICH
shows rapid onset, whereas cerebral ischemia may present with TIA. Signs of increased ICP
and edema (headache, vomiting, hiccups, seizures, and disturbance of consciousness) may also
be misleading and should not be considered in the differential diagnosis, although rapid
progression of symptoms and impaired consciousness occur more often after ICH.
C.1. Diagnosis of ICH
• ICH is a medical emergency of the highest degree with frequent early neurological
deterioration or death. Vomiting, early change in level of consciousness and high
elevation of blood pressure in a patient with acute stroke suggest ICH.
• CT of the head is the imaging procedure of choice in the initial Assessment of suspected
ICH.
• Angiography should be considered for all patients without a clear cause of hemorrhage
who are surgical candidates, particularly young, normotensive patients who are clinically
stable.
• Angiography is not required for older hypertensive patients who have a hemorrhage in
the basal ganglia, thalamus, cerebellum, or brain stem and in whom CT findings do not
suggest a structural lesion. Older patients with deep hemorrhages die or have severe
morbidity related to the hemorrhage and are not candidates for angiography.
• Timing of cerebral angiography depends on the patient’s clinical state and the
neurosurgeon’s judgment concerning the urgency of surgery, if needed.
• MRI and MRA are helpful and may obviate the need for contrast cerebral angiography in
selected patients. They should also be considered to look for cavernous malformations in
normotensive patients with lobar hemorrhages and normal angiographic results who are
surgical candidates.
23
Algorithm:
Table 14. Medical history, examination and diagnostic measures in the ED
No
Yes
Ттий
м
No
Yes
No
General care: Electrolyte
balance, air way, fluid
intake, slight BP reduction
if hypertensive, treatment
of increased ICP, and
treatment of secondary
complications (pneumonia,
DVT, urinary tract
infection), nursing care
Intracerebral or
intraventricular
hemorrhage:
Medical history, general and
neurologic exam, blood and
urine studies, ECG, head
CT or MR scan, consider
cerebral angiography, chest
X ray
Other causes of ICH:
AVM, aneurysm, angioma,
fibrinolytics, vasculitis,
thrombocytopenia, bleeding
diathesis, hemophilia, brain
tumors, head trauma, etc.
Workup and treatment as
specifically indicated
Location of the hemorrhage and associated symptoms
Supratentorial
deep
hemorrhage
Lobar
intracerebral
hemorrhage
Basal ganglia
hemorrhage
Intraventricular
hemorrhage
Brain stem
hemorrhage
Cerebellar
hemorrhage
Profound neurologic deficit
associated with brain stem
compression and a large(>3см)
hemorrhage with or without
intraventricular extention
A small hemorrhage on CT scan
with or without neurologic deficit
and little evidence of increased ICP
or brain stem involvement
A focal neurologic deficit referable to
the hemorrhage with minimal signs
of brain stem dysfunction but a
moderate to large lesion on CT scan
Conservative treatment as
outlined above, general care
Head CT: Small
hematoma with
stable
neurologic
course,
unimpaired
consciousness,
and no signs of
brain stem
compression
Moderate or
large sized
hematoma with
signs of brain
stem
compression or
deterioration
Consider cerebral angiography
and surgical evacuation of the
hematoma in those patients
who survive the initial days and
improve
Conservative treatment as
outlined above (consider
cerebral angiography if the
cause of hemorrhage not
obvious
Consider immediate cerebral
angiography and surgical
treatment
Surgical
candidate?
Surgical
candidate?
Progressi
24
Explanation
History reveiw
set the time when the patient
was last known to be
neurologically normal
Initial symptoms, its progression
Vascular risk factors High blood pressure, diabetes mellitus, hyperlipidemia, smoking
Drug consumption Anticoagulants (heparin, warfarin), antiplatelet drugs (aspirin,
clopidogrel), decongestives, hypotensive drugs, weight lowering,
sympathomimetic substances
Resent trauma, surgery Carotid surgery, stent
Dementia
Alcohol and narcotic substances cocaine and other sympathomimetic substances
Seizures
Liver disorders Changes in coagulation factors
Cancer and hematological
disorders
Changes in coagulation factors
Examination
General condition and vital
functions
Fever associated with early deterioration and complications
The risk of stroke its complications and mortality is directly
related to the degree of hypertension
Immediate and accurate
neurologic examination
Needed assessment of severity of speech and motor
impairments by NIH and NINDS scale, and unconsciousness by
GCS
Blood and urine analysis
Blood cell count, electrolytes,
creatinine, urea, glucose, nitrogen
High creatinine and glucose levels may potentiate volume
expanding hematoma and poor outcome
Coagulation factors: PT, INR,
pATT
Warfarin associated hemorrhage may rapidly expand,so is high
risk factor of morbidity and mortality
Toxicology test: check cocaine,
sympathomimetic substances
Cocaine and other sympathomimetic substances mostly caused
cerebral hemorrhages
Urine test
Other analyses
ECG Assessment of heart failure and previous myocardial infarction,
and Assessment of cardiac ejection fraction
Chest X-ray
Brain CT or MRI
C.2. Treatment of acute ICH
General principles of caring for patients with ICH
1. Place patient on bed rest in quiet room
2. Provide ongoing monitoring of neurologic status (level of consciousness, focal deficit, GCS)
3. Consider cardiac monitoring
4. Elevate head end of bed to 30 degrees
5. Prevent straining (stool softeners and antitussive agents as needed)
6. Provide oral nutrition for alert patients with intact gag reflex
7. 7. Provide enteral nutrition with nasogastric tube for patients with decreased level of
consciousness or impaired gag reflex
8. Maintain normovolemia and normal sodium level by starting with administration of 2-3
liters/day solutions of 0.9 normal saline
9. Mildly sedate patient if agitated (phenobarbital 30-60 mg 2 times a day)
25
10. Control mild pain with acetaminophen or propoxyphene and severe pain with codeine(60mg,
IM or PO,every 3-4 hr); use morphine (1-2 mg IV) only as last resort
Reduce BP conservatively and careful monitoring if patient has extremely increasedBP
12. Treat increased ICP as needed
C.2.1. Airway and Oxygenation
Although intubation is not required for all patients, airway protection and adequate ventilation are
critical. Patients who exhibit a decreasing level of consciousness or signs of brain stem
dysfunction are candidates for aggressive airway management. Intubation should be guided by
imminent respiratory insufficiency rather than an arbitrary cutoff such as a specific Glasgow
Coma Scale (GCS) score. Intubation is indicated for insufficient ventilation as indicated by
hypoxia (pO2<60 mm Hg or PCO2>50 mm Hg) or obvious risk of aspiration with or without
impairment of arterial oxygenation. Orotracheal intubation should be performed carefully,
following institutional protocols such as maximal preoxygenation and administration of drugs to
avoid reflex arrhythmias and/or blood pressure derangement, eg, atropine, thiopental,
midazolam, propofol, and succinylcholine. Precautions should always be taken to prevent
aspiration of gastric contents. All patients with endotracheal tubes receive nasogastric or
orogastric tubes to prevent aspiration and are monitored for cuff pressure every 6 hours.
Endotracheal tubes with soft cuffs can generally be maintained for ≤2 weeks. In the presence of
prolonged coma or pulmonary complications, elective tracheostomy should be performed after
≈2 weeks. Oxygen should be administered to all patients presenting with a possible ICH.
C.2.2. Medical treatment
– In the ICH associated with coagulopathies and severe thrombocytopenia should be
administrated appropriate coagulation factors and platelets concentrate (6-8 unit, IV
infusion),
– In patients with ICH associated with warfarin therapy (increased INR) for cardioembolic
cerebral infarction, warfarin should be discontinued and given vitamin “K” 10-20 mg, or
fresh frozen plasma, or particularly recombinant activated factor VIIa within 3 hours of
onset of symptoms,
– In heparin associated ICH , patient should be initiated on Protamine sulfate and its
dosage is 1 mg to every 100 mg heparin and depended on discontinuation time of
heparin infusion (protamine sulfate 5mg/min, IV, maximal dose less than 50mg),
– If ICH occurred in association with fibrinolytic therapy, necessary administration of blood
transfusion, Recombinant activated Factor VII, cryoprecipitate, platelets (6-8 unit) etc
may be initiated.
C.2.3. Blood Pressure Management
Table 15. Blood Pressure Management in ICH
High blood pressure
Labetalol 5–100 mg/h by intermittent bolus doses of
10–40 mg or continuous drip (2–8 mg/min)
Esmolol 500 µg/kg as a load; maintenance use, 50–
200 µg/kg/min
Nitroprusside 0.5–10 µg/kg/min
Hydralazine 10–20 mg Q 4–6 h
26
Enalapril 0.625–1.2 mg Q 6 h as needed
Low blood pressure
Volume replenishment is the first line of approach. Isotonic saline or colloids can be used and
monitored with central venous pressure or pulmonary artery wedge pressure. If hypotension
persists after correction of volume deficit, continuous infusions of pressors should be
considered, particularly for low systolic blood pressure such as <90 mm Hg.
Phenylephrine 2–10 µg/kg/min
Dopamine 2–20 µg/kg/min
Norepinephrine Titrate from 0.05–0.2 µg/kg/min
Nitroprusside, the most commonly used agent for severe elevations of blood pressure, is a
vasodilatory agent that theoretically can increase cerebral blood flow and thereby intracranial
pressure. This possible disadvantage has yet to be demonstrated in a clinical study.
C.2.4. Surgical Removal of ICH
The decision about whether and when to operate remains controversial. Patients with small
hemorrhages (<10 мл) or minimal neurological deficits should be treated medically because they
generally do well with medical treatment alone. Patients with a GCS score ≤4 should also be
treated medically because they uniformly die or have extremely poor functional outcome that
cannot be improved by surgery. Patients with cerebellar hemorrhage >3 cm in diameter who are
neurologically deteriorating or who have brain stem compression and hydrocephalus from
ventricular obstruction should have surgical removal of the hemorrhage as soon as possible.
Stereotactic aspiration may be associated with better outcomes than standard craniotomy for
moderate-sized cerebellar hemorrhages, but this hypothesis has yet to be tested in a
randomized study. Young patients with large lobar hemorrhages (≥50 мл) who deteriorate
during observation often undergo surgical removal of the hemorrhage. However, the efficacy of
this approach is supported only by the small endoscopic study of Auer and colleagues. An ICH
associated with a structural lesion such as an aneurysm or a vascular malformation may be
removed if the patient has a chance for a good outcome and the structural vascular lesion is
surgically accessible. Ultra-early removal of ICH by localized, minimally invasive surgical
procedures is promising but untested.
Table 16. Recommendations for Surgical Treatment of ICH
Nonsurgical candidates
1. Patients with small hemorrhages (<10 мл) or minimal neurological deficits).
2. Patients with a GCS score ≤4. However, patients with a GCS score ≤4 who have a cerebella
hemorrhage with brain stem compression may still be candidates for lifesaving surgery i
certain clinical situations.
Surgical candidates
27
1. Patients with cerebellar hemorrhage >3 cm who are neurologically deteriorating or who haveve
brain stem compression and hydrocephalus from ventricular obstruction should have surgica
removal of the hemorrhage as soon as possible.
2. ICH associated with a structural lesion such as an aneurysm, arteriovenous malformation, o
cavernous angioma may be removed if the patient has a chance for a good outcome and thehe
structural vascular lesion is surgically accessible).
3. Young patients with a moderate or large lobar hemorrhage who are clinically deteriorating.
Best therapy is still unclear.
D. Management of Aneurysmal Subarachnoid Hemorrhage
Subarachnoid hemorrhage occurs when the site of hemorrhage in the subarachnoid spaces
surrounding the brain. Aneurysmal SAH is caused by rupture of arterial and AVM, and other
etiological factors. Therefore SAH is divided into clinical forms: Aneurysmal SAH and nonaneurysmal SAH.
• Arterial aneurysm -80%,
• AVM -5% (angioma, dural arteriovenous fistula),
• Other rare causes-5% (hypertension, head trauma, arteritis, dissection, coagulation
disorders, hematologic diseases, sickle cell anemia),
• Unknown causes- 10%
• Non-aneurysmal SAH, mostly in the perimesencephalic cisterns – 10%
D.1. Manifestations and Diagnosis of SAH
• SAH is a medical emergency that is frequently misdiagnosed. A high level of suspicion
for SAH should exist in patients with acute onset of severe headache.
• CT scanning for suspected SAH should be performed, and lumbar puncture for analysis
of CSF is strongly recommended when the CT scan is negative.
• Selective cerebral angiography should be performed in patients with SAH to document
the presence and anatomic features of aneurysms.
• MRA and CTA may be considered when conventional angiography cannot be performed
in a timely fashion.
28
Table 17. Clinical grades of SAH
Wold Federation of Neurosurgery,
SAH grading scale
Hunt-Hess scale
l GCS score Motor deficit Grade Criteria
I 15 Absent I Asymptomatic, minimal headache, stiff
neck
II 14-13 Absent II Moderate to severe headache, stiff
neck, cranial nerve palsy, no focal
neurologic symptoms
III 14-13 Present III Confusion, slight neurologic symptoms
IV 12-7 Present or absent IV Stupor, moderate-severe hemiparesis,
possibly early decerebrate signs
V 6-3 Present or absent V Deep coma
Sudden severe headache,
nauseas, vomiting,
unconscious, meningismus,
focal neurological deficits
Urgent CT scan
(noncontrast)
If it is negative: CSF
xanthochromia?
Check respiratory system
and CVS. FBC,
Examinations, anamnesis
ASAH
If clinically
suspecting ASAH
Aneurysm found:
– Diagnosis: AneurysmalSAH
Angiography
Not found aneurysm:
1. CT positive, CSF-xantochromia: no
aneurysmal SAH
2.If CT and CSF negative check other causes
Management algorithm 1
29
D.2. Medical management of SAH
General principles of caring for patients with SAH
1. Place patient on bed rest in quiet room
2. Provide ongoing monitoring of neurologic status (level of consciousness, focal deficit, GCS)
3. Consider cardiac monitoring
4. Elevate head end of bed 30 degrees
5. Prevent straining (stool softeners and antitussive agents as needed)
6. Provide oral nutrition for alert patients with intact gag reflex
7. Provide enteral nutrition with nasogastric tube for patients with decreased level of
consciousness or impaired gag reflex
8. Maintain normovolemia and normal sodium level by starting with administration of 2-
3liters/day solutions of 0.9 normal saline
9. Mildly sedate patient if agitated (phenobarbital 30-60 mg 2 times a day)
10. Control mild pain with acetaminophen or propoxyphene and severe pain with
codeine(60mg, IM or PO, every 3-4 hr); use morphine (1-2 mg IV) only as last resort
11. Reduce BP conservatively and careful monitoring if patient has extremely increased BP
12. Treat increased ICP as needed
The following algorithm shows a general guidance of treatment in SAH
Treatment algorithm
ED care, CPR, FBC, Urine test, ECG
Diagnosis of level (Hunt-Hess grade or
WFNS)
– Bed rest, head lift 30 degrees
– Monitoring: neurologic examination,
CVS, RS, fluid balance (intravenous 0.9%
NaCl) and ICP managing
– If GCS<8 urgent intubation, central vein
and arterial catetherization
– Neurosurgeon consult
– If there is slight focal neurologic
symptoms  manage pain (Fentanyl,
50mcg/1сс, st), if sedation needs Propofol
perfusion
– Fisher scale  prevent vasospasm
Nimodipine 60mg, PO every 4hours or
iv in first two hours 1mg/hr, next 2mg/hr
(keeping dosage: 1~3mg/hr)
– Monitoring BPNicardipine or Labetalol
iv 10-20 mg in 10-20 min if bradicardy
in Labetalol  hydralazine or ACEblocker
– For prevent seizure Valproate 400mg/8hr
– For prevention of gastric ulcer Famotidine
(20mg/12hr)
– Special socks for prevention of deep vein
thrombosis
Conservative therapy
in 4-5 gradeif
improve till 1-3 grade
in first 3 days urgent
surgery
In 1-3 grade if
patient condition
is stable urgent
surgery
Surgical therapy:
Usually: surgery (in 3-14 days because of
vasospasm don’t do surgery)
Rarely: endovascular coil
Post-operative management
30
D.3. Surgical or Endovascular Treatment of Ruptured Aneurysms
1. Surgical clipping or endovascular coiling should be performed to reducethe rate of rebleeding after aneurysmal SAH.
2. Wrapped or coated aneurysms and incompletely clipped or coiled aneurysms have an
increased risk of re-hemorrhage compared with those that are completely occluded and
therefore require long-term follow-up angiography. Complete obliteration of the
aneurysm is recommended whenever possible.
3. For patients with ruptured aneurysms judged by an experienced team of
cerebrovascular surgeons and endovascular practitioners to be technically amenable to
both endovascular coiling and neurosurgical clipping, endovascular coiling can be
beneficial. Nevertheless, it is reasonable to consider individual characteristics of the
patient and the aneurysm in deciding the best means of repair, and management of
patients in centers offering both techniques is probably indicated.
4. Although previous studies showed that overall outcome was not different for early
versus delayed surgery after SAH, early treatment reduces the risk of re-bleeding after
SAH, and newer methods may increase the effectiveness of early aneurysm treatment.
Early aneurysm treatment is reasonable and is probably indicated in the majority of
cases.
D.4. Medical Measures to Prevent Re-bleeding After SAH
• Blood pressure should be monitored and controlled to balance the risk of stroke,
hypertension-related re-bleeding, and maintenance of cerebral perfusion pressure.
• Bed rest alone is not enough to prevent re-bleeding after SAH. It may be considered a
component of a broader treatment strategy, along with more definitive measures.
• Although older studies demonstrated an overall negative effect of antifibrinolytics, recent
evidence suggests that early treatment with a short course of antifibrinolytic agents
(EACA 24-36 g/day 1000ml of 5% dextrose solution, or tranexamic acid 1 g IV or 1.5 g
orally 4-6 times daily) combined with a program of early aneurysm treatment followed by
discontinuation of the antifibrinolytic and prophylaxis against hypovolemia and
vasospasm may be reasonable, but further research is needed. Furthermore,
antifibrinolytic therapy to prevent rebleeding may be considered in certain clinical
situations, in patients with a low risk of vasospasm and/or a beneficial effect of delaying
surgery.
D.5. Management of Cerebral Vasospasm
• Oral nimodipine is indicated to reduce poor outcome related to aneurysmal SAH. The
value of other calcium antagonists, whether administered orally or intravenously, remains
uncertain.
• Treatment of cerebral vasospasm begins with early management of the ruptured
aneurysm, and in most cases, maintaining normal circulating blood volume and avoiding
hypovolemia are probably indicated.
• One reasonable approach to symptomatic cerebral vasospasm is volume expansion,
induction of hypertension, and hemodilution (triple-H therapy).
31
• Alternatively, cerebral angioplasty and/or selective intra-arterial vasodilator therapy may
be reasonable after, together with, or in the place of triple-H therapy, depending on the
clinical scenario.
32
E. Management of complications in Strokes
E.1. Therapy of elevated Intracranial Pressure and Hydrocephalus
ICP is considered a major contributor to mortality after Stroke; thus, its control is essential. ICP
may be managed through osmotherapy, controlled hyperventilation, and barbiturate coma.
Elevated ICP is defined as intracranial pressure ≥20 mm Hg for >5 minutes. A therapeutic goal
for all treatment of elevated ICP is ICP <20 mm Hg and cerebral perfusion pressure (CPP) >70
mm Hg. Optimal head position (raised 15-30) can be adjusted according to ICP values. Patients
with suspected elevated ICP and deteriorating level of consciousness are candidates for
invasive ICP monitoring. The GCS level that requires ICP monitoring should be based on rate of
decline and other clinical factors such as CT evidence of mass effect and hydrocephalus. In
general, ICP monitors should be placed in patients with a GCS score of <9 and all patients
whose condition is thought to be deteriorating due to elevated ICP. The type of device depends
on availability, experience, and situation. Intraventricular ICP monitors and
intraparenchymalfiberoptic ICP devices are 2 commonly used methods of monitoring ICP.
In addition to the mass effect of the hematoma, secondary hydrocephalus may contribute to
elevated ICP. Ventricular drains should be used in patients with or at risk for hydrocephalus.
Drainage can be initiated and terminated according to clinical performance and ICP values.
Because of infectious complications, external drainage devices must be checked regularly, and
duration of placement ideally should not exceed 7 days. Use of anti-infectious prophylaxis is
recommended.
Although universally accepted standardized therapy protocols for elevated ICP have not been
established, The beneficial effect of sustained hyperventilation on ICP is unresolved. In theory,
reduction of ICP by hyperventilation ceases when the pH of cerebrospinal fluid (CSF) reaches
equilibrium. In practice, this may not occur for many hours. Some authors believe that prolonged
hyperventilation has a beneficial effect on brain water volume. As with osmotherapy, adverse
rebound effects can occur if normal ventilation is resumed too quickly. When hyperventilation is
deemed no longer necessary, gradual normalization of serum PCO2 should occur over a 24- to
48-hour period. In general, if hyperventilation is instituted for elevated ICP, PCO2 should be
maintained between 30 and 35 mm Hg until ICP is controlled. In addition, most patients will
require sedation with agents such as propofol, benzodiazepines, or morphine and treatment with
intermittent muscular paralysis.
E.1.2. Management of ICP
• Osmotherapy: The first medical line of defense is osmotherapy. However, it should not be
used prophylactically. Mannitol 20% (0.25–0.5 g/kg every 4 h) or glycerol (10%, 250ml every
6 h) are reserved for patients with progressively increasing ICP values, or clinical
deterioration associated with mass effect. Due to its rebound phenomenon, mannitol is
recommended for only ≤5 days. To maintain an osmotic gradient, furosemide (10 mg Q 2–8
h) may be administered simultaneously with osmotherapy. Intravenous hypertonic saline
solutions (NaCL 23.4%, 30ml) are probably similarly effective. Serum osmolality should be
measured twice daily in patients receiving osmotherapy and targeted to ≤310 mOsm/L.
• Corticosteroids in stroke are generally avoided because multiple potential side effects must
be considered and clinical studies have not shown benefit.
33
• Hyperventilation: Hypocarbia causes cerebral vasoconstriction. Reduction of cerebral blood
flow is almost immediate, although peak ICP reduction may take up to 30 minutes after pCO2
is changed. Reduction of pCO2 to 35–30 mm Hg, best achieved by raising ventilation rate at
constant tidal volume (12–14 mL/kg), lowers ICP 25% to 30% in most patients. Failure of
elevated ICP to respond to hyperventilation indicates a poor prognosis.
• Muscle relaxants: Neuromuscular paralysis in combination with adequate sedation can
reduce elevated ICP by preventing increases in intrathoracic and venous pressure associated
with coughing, straining, suctioning, or “bucking” the ventilator. Nondepolarizing agents, such
as vecuronium or pancuronium, with only minor histamine liberation and ganglion-blocking
effects, are preferred in this situation. Patients with critically elevated ICP should be
pretreated with a bolus of a muscle relaxant before airway suctioning. Alternatively, lidocaine
may be used for this purpose.
• If elevated ICP cannot be controlled with the above mentioned treatment alternatives,
induced barbiturate coma may be instituted. However, high-dose barbiturate therapy should
be viewed as an option and not part of a standardized algorithm in the treatment of elevated
ICP in patients with stroke. Short-acting barbiturates such as thiopental are known to
effectively reduce elevated ICP. The effect is presumably mediated through reduction of
cerebral blood flow and volume. In addition to reducing the volume of the normal brain,
barbiturates reduce brain swelling, perhaps as a result of mild systemic hypotension, and
may act as free radical scavengers. The complications of high-dose barbiturate administration
(safe limit: ≈10 mg/kg per day) include hypotension, which is most pronounced at the time of
bolus administration, and possible predisposition to infection. Systemic hypotension mainly
results from decreased venous tone, baroreflex tone, and sympathetic activity.
Cardiovascular side effects may be aggravated by concomitant dehydration promoted by
osmotherapy and diminished cardiac filling pressures. Maximal reduction in cerebral
metabolism is accompanied by electrocerebral silence (continuous EEG recording). Since
some tolerance develops with continued administration of barbiturate, use of multiple small
boluses may be considered (0.3 to 0.6 mg/kg).
Management of Hydrocephalus:
• Temporary or permanent CSF diversion is recommended by external ventricular drainage
in symptomatic patients with chronic hydrocephalus after SAH.
• Ventriculostomy can be beneficial in patients with hydrocephalus and diminished level of
consciousness after acute SAH.
Management of Seizures
• The administration of prophylactic anticonvulsants may be considered in the immediate
post-hemorrhagic period
• The routine long-term use of anticonvulsants is not recommended but may be
considered for patients with risk factors such as prior seizure, parenchymal hematoma,
infarct, or middle cerebral artery aneurysms
34
Algorithm for management ICP
Management of Hyponatremia
• Avoid increased use of hypotonic solutions
• Test forany changes in antidiuretic hormone level and sodium loss syndromes.
(Hypotonic hyponatremia, extracellular dehydration)
• If sodium loss syndromes caused by hypovolemia: for correcting hyponatremia use
isotonic sodium solution, Ringer lactate or colloid solutions (central vein pressure must
be 8-12mm Hg)
• If there are changes in antidiuretic hormone levels, reduce intake of fluids (less than 1
litre per day) and use Lasix(Ferusomide) daily 40mg or Demeclocycline 300-600 mg
twice a day PO
35
• Decide about including in the complex therapy Fludrocortisone Acetateby 1mg twice a
day.
• Decide in rare case of hyponatriemia (<120 mEq/l) use of 3% sodium chloride 25-
50ml/hr.
• Avoid quick correction of sodium level in hyponatremia (during 24hours ≤20mEq/lor 1,5-
2mEq/l/hr) , to avoid potential danger of central pontinemyelinolysis (CPM) with rapid
correction.
E.2. Prevention and management of other complications in Strokes
• Infections after strokes should be treated with appropriate antibiotics. Prophylactic
administration of antibiotics is not recommended;
• Early rehydration and graded compression stockings / pneumatic compression devices
are recommended to reduce the incidence of venous thromboembolism;
• Early mobilization is recommended to prevent complications such as aspiration
pneumonia, DVT and pressure ulcers;
• It is recommended that low-dose subcutaneous heparin or low molecular weight
heparins should be considered for patients at high risk of DVT or pulmonary embolism;
• Administration of anticonvulsants is recommended to prevent recurrent post-stroke
seizures. Prophylactic administration of anticonvulsants to patients with recent stroke
who have not had seizures is not recommended;
• An assessment of falls risk is recommended for every stroke patient;
• Calcium/vitamin-D supplements are recommended in stroke patients at risk of falls;
• In stroke patients with urinary incontinence, specialist assessment and management is
recommended;
• Swallowing assessment is recommended as a routine, but there are insufficient data to
recommend a specific approach for treatment;
• Oral dietary supplements are only recommended for non-dysphagic stroke patients who
are malnourished;
• Early commencement of nasogastric (NG) feeding (within 48 hours) is recommended in
stroke patients with impaired swallowing;
• It is recommended that percutaneous enteral gastrostomy (PEG) feeding should not be
considered in stroke patients in the first 2 weeks.
F. Rehabilitation (see special guideline worked out on it)
Even with optimal stroke unit care including thrombolysis, fewer than one third of patients
recover fully from stroke. Rehabilitation aims to enable people with disabilities to reach and
maintain optimal physical, intellectual, psychological and/or social function. Goals of
rehabilitation can shift from initial input to minimize impairment to more complex
interventions designed to encourage active participation.
Setting for rehabilitation
• Admission to a stroke unit with rehabilitation facility is recommended for acute stroke
patients to receive coordinated multidisciplinary rehabilitation;
• Early initiation of rehabilitation is recommended;
36
• It is recommended that early discharge from stroke unit is possible in medically stable
patients with mild or moderate impairment provided that rehabilitation is delivered in
the community by a multidisciplinary team with stroke expertise;
• Tricyclic or anticonvulsant therapy are recommended to treat post-stroke neuropathic
pain in selected patients;
• Drug therapy and non-drug interventions are recommended to improve cognitive
function and mood in depressive patients;
• It is recommended to continue rehabilitation after discharge during the first year after
stroke;
• It is recommended to increase the duration and intensity of rehabilitation;
The results from stroke unit trials favor coordinated multidisciplinary teams of staff with
expertise in stroke care. The composition of these teams is not formally prescribed, but
usually includes stroke physicians, neurosurgeons, physiatrists, neuroradiologists (including
interventionists), vascular surgeons, nutritionists, cardiologists, nursing staff,
physiotherapists, occupational therapists, and speech and language therapists.
H. Prevention
H.1. Primary prevention
The aim of primary prevention is to reduce the risk of stroke in asymptomatic people.
Management of vascular risk factors
• Provide educational programs to increase awareness of stroke at the population level;
• Provide educational programs to increase stroke awareness among professionals
(paramedics/emergency physicians);
• Provide a community awareness for prevention of stroke and urgent referral to
emergency medical service if stroke occurs;
• Blood pressure should be checked regularly. It is recommended that high blood
pressure should be managed with lifestyle modification and individualized
pharmacological therapy aiming at normal levels of 120/80 mmHg. For prehypertensive
(120-139/80-90 mmHg) with congestive heart failure, MI, diabetes, or chronic renal
failure antihypertensive mediation is indicated;
• The relationship between hypertension and aneurysmal SAH is uncertain. However,
treatment of high blood pressure with antihypertensive medication is recommended to
prevent ischemic stroke, intracerebral hemorrhage, and cardiac, renal, and other end-organ
injury.
• Careful control of the anticoagulation level in patient’s warfarin therapy reduces the risk of
subsequent ICH.
• Careful selection of patients for thrombolytic treatment for acute myocardial infarction and
acute ischemic stroke should result in a decline in ICH rates.
• Blood glucose should be checked regularly. It is recommended that diabetes should be
managed with lifestyle modification and individualized pharmacological therapy. In
diabetic patients, high blood pressure should be managed intensively aiming for levels
below 130/80 mmHg. Where possible, treatment should include an angiotensin
converting enzyme inhibitor or angiotensin receptor antagonist;
37
• Blood cholesterol should be checked regularly. It is recommended that high blood
cholesterol (e.g. LDL> 150 mg/dl [3.9 mmol/l]) should be managed with lifestyle
modification and a statin;
• It is recommended to quit cigarette smoking;
• Regular physical activity is recommended;
• A diet low in salt and saturated fat, high in fruit and vegetables and rich in fiber is
recommended; avoidance of heavy alcohol and use of sympathomimetic drugs may
decrease risk of ICH
• Subjects with an elevated body mass index are recommended to take a weight-reducing
diet;
• Antioxidant vitamin supplements are not recommended;
• Hormone replacement therapy is not recommended for the primary prevention of stroke;
A healthy lifestyle, consisting of abstinence from smoking, low-normal body mass index,
regular exercise and healthy diet, is associated with a reduction in strokes.
Antithrombotic therapy
• Low-dose aspirin is recommended in women aged 45 years or more who are not at
increased risk for intracerebral hemorrhage and who have good gastro-intestinal
tolerance;
• It is recommended that low-dose aspirin may be considered in men for the primary
prevention of myocardial infarction; however, it does not reduce the risk of ischemic
stroke;
• Antiplatelet agents other than aspirin are not recommended for primary stroke
prevention;
• Aspirin may be recommended for patients with non-valvular AF who are younger
than 65 years and free of vascular risk factors;
• Unless contraindicated, either aspirin or an oral anticoagulant (international
normalized ratio [INR] 2.0-3.0) is recommended for patients with non-valvular AF
who are aged 65-75 years and free of vascular risk factors;
• Unless contraindicated, an oral anticoagulant (INR 2.0–3.0) is recommended for
patients with non-valvular AF who are aged >75, or who are younger but have risk
factors such as high blood pressure, left ventricular dysfunction, or diabetes mellitus;
• It is recommended that patients with AF who are unable to receive oral
anticoagulants should be offered aspirin;
• It is recommended that patients with AF who have mechanical prosthetic heart
valves should receive long-term anticoagulation with a target INR based on the
prosthesis type, but not less than INR 2.0–3.0;
• Low dose aspirin is recommended for patients with asymptomatic internal carotid
artery (ICA) stenosis >50% to reduce their risk of vascular events;
Carotid surgery and angioplasty
• Carotid surgery is not recommended for asymptomatic individuals with significant
carotid stenosis (60-99%), except in those at high risk of stroke;
• Carotid surgery is recommended for symptomatic individuals with significant carotid
stenosis (>70%),
38
• Carotid angioplasty, with or without stenting, is not recommended for patients with
asymptomatic carotid stenosis;
• It is recommended that patients should take aspirin before and after surgery;
H. 2. Secondary prevention
Optimal management of vascular risk factors
• It is recommended that blood pressure be checked regularly. Blood pressure
lowering is recommended after the acute phase of strokes;
• It is recommended that blood glucose should be checked regularly. It is
recommended that diabetes should be managed with lifestyle modification and
individualized pharmacological therapy;
• In patients with type 2 diabetes who do not need insulin, treatment with pioglitazone
is recommended after stroke;
• Statin therapy is recommended in subjects with non-cardioembolic stroke;
• It is recommended to quit cigarette smoking;
• It is recommended that heavy use of alcohol be discouraged;
• Regular physical activity is recommended;
• A diet low in salt and saturated fat, high in fruit and vegetables, and rich in fiber is
recommended;
• Subjects with an elevated body mass index are recommended to adopt a weightreducing diet;
• Antioxidant vitamin supplements are not recommended;
• Hormone replacement therapy is not recommended for the secondary prevention;
• Sleep-disordered breathing such as obstructive sleep apnoea is recommended to be
treated with continuous positive airway pressure breathing;
• It is recommended that endovascular closure of PFO be considered in patients with
cryptogenic stroke and high risk PFO;
Antithrombotic therapy
• It is recommended that patients receive antithrombotic therapy;
• It is recommended that patients not requiring anticoagulation should receive
antiplatelet therapy. Where possible, combined aspirin and dipyridamole, or
clopidogrel alone, should be given;
• The combination of aspirin and clopidogrel is not recommended in patients with
recent ischemic stroke, except in patients with specific indications (e.g. unstable
angina or non-Q-wave MI, or recent stenting); treatment should be given for up to 9
months after the event;
• It is recommended that patients who have a stroke on antiplatelet therapy should be
re-evaluated for pathophysiology and risk factors;
• Oral anticoagulation (Warfarin 5mg; INR 2.0–3.0) is recommended after ischemic
stroke associated with AF. Oral anticoagulation is not recommended in patients with
co-morbid conditions such as falls, poor compliance, uncontrolled epilepsy, or
gastrointestinal bleeding. Increasing age alone is not a contraindication to oral
anticoagulation;
• It is recommended that patients with cardioembolic stroke unrelated to AF should
receive anticoagulants (INR 2.0-3.0) if the risk of recurrence is high;
39
• It is recommended that anticoagulation should not be used after non-cardio-embolic
ischemic stroke, except in some specific situations, such as aortic atheromas,
fusiform aneurysms of the basilar artery, cervical artery dissection, or patent foramen
ovale in the presence of proven deep vein thrombosis (DVT) or atrial septal
aneurysm;
• It is recommended that combined low dose aspirin and dipyridamole should be given
if oral anticoagulation is contraindicated;
Surgery and angioplasty
• Carotid endarterectomy (CEA) is recommended for patients with 70–99% stenosis.
CEA should only be performed in centers with a perioperative complication rate (all
strokes and death) of less than 6%;
• It is recommended that CEA be performed as soon as possible after the last
ischemic event, ideally within 2 weeks;
• It is recommended that CEA may be indicated for certain patients with stenosis of
50–69%; males with very recent hemispheric symptoms are most likely to benefit.
CEA for stenosis of 50–69% should only be performed in centers with a perioperative
complication rate (all stroke and death) of less than 3%;
• CEA is not recommended for patients with stenosis of less than 50%;
• It is recommended that patients remain on antiplatelet therapy both before and after
surgery;
• Carotid percutaneous transluminal angioplasty and/or stenting (CAS) is only
recommended in selected patients. It should be restricted to the following subgroups
of patients with severe symptomatic carotid artery stenosis: those with contraindications to CEA, stenosis at a surgically inaccessible site, re-stenosis after earlier
CEA, and post-radiation stenosis. Patients should receive a combination of
clopidogrel and aspirin immediately before and for at least 1 month after stenting;
• It is recommended that endovascular treatment may be considered in patients with
symptomatic intracranial stenosis;
40
I. Application of the guidelines for management of stroke
In each level of medical organizations
The using of the guidelines for management of acute stroke into each level of medical
organizations should be needed to provide the next requirements (table 17).
Table 17. Requirements for managing acute stroke patients in each hospital level
Requirements for
managing acute
stroke patients
State central
hospitals
(3rdlevel)
Zonal diagnostic
centers, aimag and
district hospitals
(2nd level)
Soumon
hospitals
(1st level)
Emergency medical
service
(Recognize the
signs of stroke using
the “Face-ArmSpeech Test)
Transport the patient
quickly to stroke unit or
emergency department
Transport the patient
quickly to
neurological or
emergency
department
Transport the
patient to primary
care unit
Investigation and
diagnostic actions
Perform neurologic
and cardiologic
assessments; Brain CT
or MRI, ECG, TCD;
Lab.tests: complete
blood analysis and
platelet count, PT or
INR, PTT, Serum
electrolytes, blood
glucose, CRP or ESR,
Hepatic and renal
chemical analysis
Perform neurologic
and cardiologic
assessments; Brain
CT, ECG, TCD;
Lab.tests: complete
blood analysis and
platelet count; PT or
INR, PTT, Serum
electrolytes, blood
glucose, CRP or
ESR, Hepatic and
renal chemical
analysis
Recognize the
signs of stroke
using the “FaceArm-Speech Test;
Lab.tests:
complete blood
analysis and
platelet count;
Order general
treatment for
stroke; Obtain
neurologist
consultation and
establish close
observation
Acute therapy Depending on stroke
type and time of
symptoms onset start
general and specific
appropriate treatment
(thrombolysis or
antiplatelet, or
anticoagulant therapy,
and neurosurgery
intervention)
Depending on stroke
type and time of
symptoms onset start
general and specific
appropriate treatment
(antiplatelet, or
anticoagulant
therapy, and
neurosurgery
intervention)
Depending on
stroke type and
time of symptoms
onset start general
and specific
appropriate
treatment
(antiplatelet
therapy)
Primary and second
prevention
Perform by the guidelines for management of stroke
41
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42

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