Guidelines for

Acute Stroke Treatment

(2010)

Stroke Society of the Philippines

Rm. 1403 14/F North Tower, Cathedral Heights Bldg. Complex
St. Luke’s Medical Center, E. Rodriguez Sr. Ave., Quezon City
Telephone No.: (632) 723-0101 Loc 5143
Telefax No.: (632) 722-5877
E-mail: ssp_secretariat@yahoo.com
Website: www.strokesocietyphil.org
 Acute Stroke Treatment
Stroke Society of the Philippines
Rm. 1403 14/F North Tower, Cathedral Heights Bldg. Complex
St. Luke’s Medical Center, E. Rodriguez Sr. Ave., Quezon City
Telephone No.: (632) 723-0101 Loc 5143
Telefax No.: (632) 722-5877
E-mail: ssp_secretariat@yahoo.com
Website: www.strokesocietyphil.org

Board of Trustees 2013-2014

President Artemio A. Roxas, Jr., MD

1st Vice-President
2nd Vice-President
Secretary
Treasurer
Public Relation Officer
Immediate Past President
Maria Cristina Z. San Jose, MD
Manuel M. Mariano, MD
Ma. Epifania V. Collantes, MD
Betty D. Mancao, MD
Raquel M. Alvarez, MD
Carlos L. Chua, MD

Members Alejandro C. Baroque II, MD

Romulo U. Esagunde, MD
Johnny K. Lokin, MD
Pedro Danilo J. Lagamayo, MD
Orlino A. Pacioles, MD
Peter P. Rivera, MD
Ma. Socorro F. Sarfati, MD
Annabelle Y. Lao-Reyes, MD
Ma. Leticia C. Araullo-De Jesus, MD

Stroke: Think Globally, Act Locally

Principles:

1. Stroke is a “brain attack”

...needing emergency management, including specific treatments and secondary and
tertiary prevention.
2. Stroke is an emergency
...where virtually no allowances for worsening are tolerated.
3. Stroke is treatable
...optimally, through proven, affordable, culturally-acceptable and ethical means.
4. Stroke is preventable
...in implementable ways across all levels of society.

The recommendations contained in this document are intended to merely guide practitioners in the prevention, treatment and rehabilitation of patients
with stroke. In no way should these recommendations be regarded as absolute rules, since nuances and peculiarities in individual patients, situations or
communities may entail differences in specific approaches. The recommendations should supplement, not replace, sound clinical judgments on a case-
to-case basis.

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­ ­
Background and Rationale for Simpli­
fied Initial Classification of Acute
Stroke Based on CLINICAL Severity*
There are various ways to classify stroke such as based
on stroke type, localization, brain and vascular terri-
tory involvement, patho-mechanism and time course.
However utilization of some of the standardized class­
ification schemes may be difficult & time-consuming
especially for non-neuroscience specialists in an acute
stroke setting.
The working committee of the first edition (1999) of the
SSP Stroke Handbook has developed a practical & local­
ly relevant initial classification scheme which is based
simply on observed severity of patient’s neurological
deficits, including level of sensorium and response to
pain. The present 2010 working committee still finds this
format useful particularly in the acute setting, reliable for
both medical and paramedical personnel and advocates
its continued use to help direct crucial actions and deci-
sions at the emergency room.
After initial stabilization & management, additional work-
ups are recommended for determination and further
classification of patients based on underlying stroke
patho-mechanism which is necessary for selection of
appropriate secondary prevention strategies.
­Definition of Stroke Severity
MILD MODERATE SEVERE
STROKE STROKE STROKE
Alert patients with Awake patient Deep stupor or
any or a combina- with significant comatose patient
tion of the follow- motor and/ or with non-purpose-
ing: sensory and/ or ful response,
visual deficit decorticate, or
1. Mild pure motor decerebrate
weakness of one or posturing to
side of the body, painful stimuli
defined as: can Disoriented,
raise arm above drowsy or light or
shoulder, has stupor with
clumsy hand, or purposeful Comatose
can ambulate with- response to patient with
out assistance painful stimuli no response to
2. Pure sensory painful stimuli
deficit
3. Slurred but intel-
ligible speech
4. Vertigo with inco-
ordination (e.g.,
gait disturbance,
unsteadiness
or clumsy hand)
5. Visual field
defects alone
or or or
NIHSS NIHSS NIHSS
score = 0 – 5 score = 6 - 21 score >22
See Guidelines See Guidelines See Guidelines carditis is suspected,
for TIA and for Moderate for Severe give antibiotics and
Mild Stroke Stroke Stroke
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Acute Stroke Treatment
Guidelines for TIA
(For detailed discussions on TIA, please see Chapter IV)
Ascertain clinical diagnosis of TIA
Management (history and physical exam are very
Priorities important)
• Exclude common stroke mimickers
Provide basic emergent supportive
care (ABCs of Resuscitation)
Monitor neuro-vital signs, BP, MAP,
RR, temperature, pupils
Perform stroke scales (NIHSS, GCS)
Perform risk stratification using the
ABCD2 Scale
Monitor and manage BP, treat if
MAP >130
Precautions:
• Avoid precipitous drop in BP (not
>15% of baseline MAP). Do not use
rapid-acting sublingual agents; when
needed, use easily titratable IV or
short acting oral antihypertensive
medication.
• Ensure appropriate hydration.
Recommended IVF - 0.9% NaCl
if needed.
Emergent • Complete blood count (CBC)
Diagnostics • Blood sugar (CBG or RBS)
• Electrocardiogram (ECG)
• PT/PTT
• Cranial MRI-DWI as soon as
possible is preferred. May do
Non-contrast Cranial CT scan if
MRI is not possible.
Non-cardio- Cardioembolic
embolic
Aspirin 160-325 Consider careful
Early mg/day. start anticoagulation
Specific as early as with IV heparin or
Treatment possible and SQ low molecular-
continue for weight heparin
14 days (LMWH) for those
at high risk for early
For secondary recurrence (e.g.,
prevention, AF with thrombus,
see under valvular heart
"Delayed disease or MI)
Management
and Treatment" or
Neuroprotection Aspirin 160-325
mg/day (if anti-
coagulation is not
possible or contra-
indicated)
Neuroprotection
If infective endo-
do not anticoagulate.

Acute Stroke Treatment
Admit to Hospital (Stroke Unit) Urgent Outpatient Work-up

Place of 1. TIA within 48 hours TIA >2 weeks (but work-ups should be
Treatment 2. Crescendo TIAs (multiple & increasing done within 24 – 48 hours)
symptoms)
3. TIA with known high risk cardiac source of
embolism, known hypercoagulable state
or symptomatic ICA stenosis
4. Patient with ABCD2 score of >3

Non-cardioembolic
(Thrombotic/Lacunar) Cardioembolic Others

Delayed Antiplatelets (aspirin, clopidogrel, Echocardiography Specialized coagulation

Management cilostazol, triflusal, dipyridamole, and/or cardiology tests such as screening
and extended-release dipyridamole + consult for hypecoagulable states
Secondary aspirin combination) (protein C, protein S,
Prevention If age <75 and PT/INR antithrombin III, fibrinogen,
Control of risk factors available, anticoagu- homocysteine) and drug
lation with warfarin screening (e.g., metam-
Recommended vascular studies (target INR: 2-3) phetamine, cocaine) can be
such as carotid ultrasound to considered for young
document extracranial stenosis. If age >75, warfarin patients with TIA especially
If this reveals >70% stenosis, refer (target INR: 2.0 when no vascular risk
to neurologist/neurosurgeon/ [1.6-2.5]) factors exist and no under-
vascular surgeon for decision- lying cause is identified
making regarding CEA or If anticoagulation is
stenting contraindicated, give If vasculitis is suspected,
antiplatelets (ASA may do ESR, ANA, Lupus
To document intracranial stenosis, 160 mg-325 mg) anticoagulant testing
recommend either TCD or MRA or
CTA Transesophangeal echo-
cardiography (TEE) to rule
out PFO

­
Guidelines for Mild Stroke

Ascertain clinical diagnosis of stroke (history and physical exam are very important)
Management • Exclude common stroke mimickers
Priorities • Provide basic emergent supportive care (ABCs of resuscitation)
• Monitor neuro-vital signs, BP, MAP, RR, temperature, pupils, O2 saturation
• Perform and monitor stroke scales (NIHSS, GCS)
• Provide O2 support to maintain O2 saturation >95%
• Monitor and manage BP; treat if MAP >130

Precautions:
• Avoid precipitous drop in BP (not >15% of baseline MAP). Do not use rapid-acting
sublingual agents; when needed use easily titratable IV or oral antihyper­tensive
medication.
• Ensure adequate hydration. Recommended IVF - 0.9% NaCl.

Emergent • Complete Blood Count (CBC)

Diagnostics • Blood Sugar (CBG or RBS)
• Electrocardiogram (ECG)
• PT/PTT
• Non-contrast CT scan of the brain or MRI-DWI as soon as possible
• If ICH, compute for hematoma volume


 Acute Stroke Treatment
Ischemic Hemorrhagic

Early Specific Non-cardioembolic

Treatment (Thrombotic, Lacunar) Cardioembolic

Aspirin 160-325 mg/day start as Consider careful anti- Early neurology and/ or
early as possible and continue coagulation with IV neuro­ surgeon consult for
for 14 days heparin or SQ low mole- all ICH is recommended
cular-weight heparin
CT-scan For secondary prevention, see (LMWH) for those high Monitor and maintain BP:
confirmed under "Delayed Management and risk with early recurrence Target MAP of 110 or SBP
Treatment" (e.g., AF with thrombus, of 160
valvular heart disease
Neuroprotection or MI) Neuroprotection

Early rehabilitation once stable or Early rehabilitation once
within 72 hours stable within 72 hours
Aspirin 160-325 mg/day
(if anticoagulation is not Give anticonvulsants for
possible or contra- clinical seizures and proven
indicated) subclinical or electrographic
seizures. Prophylactic
Neuroprotection AEDs are generally not
(Appendix V-D) recommended

Early rehabilitation once Steroids are not recom-
stable within 72 hours mended

If infective endocarditis Monitor and correct meta-
is suspected, give bolic parameters
antibiotics and do
not anticoagulate Correct coagulation/bleed-
ing abnormalities

Follow recommendations
for neurosurgical interven-
tion

For aneurysmal SAH, refer

to specific chapter

Place of
treatment Admit to Hospital: Acute Stroke unit/Regular Room

Ischemic Hemorrhagic

Delayed Non-cardioembolic
Management (Thrombotic, Lacunar) Cardioembolic
and Treatment
(Secondary Antiplatelets (aspirin, clopidogrel, Echocardiography and/ Long-term strict BP control
Prevention) cilostazol, triflusal, dipyridamole, or cardiology consult and monitoring
extended-release dipyridamole +
aspirin combination) If age <75 and PT/INR Consider contrast CT
available, anticoagula- scan, 4 vessel cerebral
Control of risk factors tion with warfarin angiogram, MRA or CTA
(target INR: 2-3) if patient is:
Recommended vascular studies
such as carotid ultrasound to If age >75, warfarin 1) <45 years old,
document extracranial stenosis. (target INR: 2.0 [1.6-2.5]) 2) normotensive
If this reveals >70% stenosis, refer 3) has lobar ICH
to neurologist/neurosurgeon/vascular If anticoagulation is 4) uncertain cause of ICH
surgeon for decision-making contraindicated, give 5) suspected to have
regarding CEA or stenting antiplatelets (ASA 160 aneurysm, AV malformation
mg-325 mg) or vasculitis
To document intracranial stenosis,
recommend either TCD or MRA
or CTA

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Acute Stroke Treatment
­
Guidelines for Moderate Stroke
Ascertain clinical diagnosis of stroke (history and physical exam are very important)
Management • Exclude common stroke mimickers
Priorities Basic emergent supportive care (ABCs of resuscitation)
Neuro-vital signs, BP, MAP, RR, temperature, pupils, oxygen saturation
Perform and monitor stroke scales (NIHSS, GCS)
Monitor and manage BP. Treat if MAP >130
Provide O2 support to maintain O2 saturation >95%
• Precaution: Avoid precipitous drop in BP (not >15% of baseline MAP). Do not use rapid-acting
sublingual agents; when needed use easily titratable IV or oral antihypertensive medication.
Identify comorbidities (cardiac disease, diabetes, liver disease, gastric ulcer, etc.)
Recognize and treat early signs and symptoms of increased ICP
Ensure adequate hydration. Recommended IVF-0.9% NaCl

Emergent • CBC with platelet count • ECG

Diagnostics • CBG or RBS • Non-contrast CT scan of brain or
• PT/PTT MRI-DWI as soon as possible
• Serum Na+ and K+ • If ICH, compute for hematoma volume

Ischemic Hemorrhagic

Early Specific Non-cardioembolic

Treatment (Thrombotic, Lacunar) Cardioembolic

If within 3 hours of stroke onset, If within 3 hours of Early neurology and/ or

consider IV recombinant tissue stroke onset, consider neurosurgical consult for all
plasminogen activator (rt-PA) and IV rt-PA and refer to ICH is recommended
refer to neuro specialist neuro specialist
Monitor and maintain BP.
CT-scan Selected patients within If within 6 hours of Target MAP = 110 mmHg
confirmed 3 – 4.5 hour time window may stroke onset and in or SBP = 160 mmH
benefit with IV recombinant tissue specialized centers,
plasminogen activator (see section consider IA thrombolysis Neuroprotection
on thrombolytic therapy)
If rt-PA ineligible or 24 Give anticonvulsants for
hours after rt-PA treat- clinical seizures and proven
ment consider either care- subclinical or electrographic
ful anticoagulation with seizures. Prophylactic
AEDs are generally not
Refer to neurologist for evaluation IV heparin or SQ recommended
& decision. LMWH for those at high
risk for early recurrence Steroids are not
If within 6 hours of stroke onset or ASA 160-325 mg/day recommended
and in specialized centers,
consider intra-arterial (IA) Neuroprotection Monitor and correct
thrombolysis metabolic parameters

Start ASA 160-325 mg 24 hours Early supportive

after rtPA treatment. rehabilitation Correct coagulation/
bleeding abnormalities
If rtPA ineligible, start Aspirin If infective endocarditis
160-325 mg/day as soon as is suspected, give Follow recommendations
possible antibiotics and do not for neurosurgical
anticoagulate intervention
Neuroprotection
Early rehabilitation once
Early supportive rehabilitation stable

Consider early decompressive For aneurysmal SAH, refer

Hemicraniectomy for large to specific chapter
malignant MCA infarction

Place of Hospital - Intensive Care Unit or Stroke Unit

Treatment

 Acute Stroke Treatment
Ischemic Hemorrhagic

Delayed Non-cardioembolic
Management (Thrombotic, Lacunar) Cardioembolic
and Treatment
(Secondary Antiplatelets (aspirin, clopidogrel, Echocardiography and/ Long-term strict BP control
Prevention) cilostazol, triflusal, dipyridamole, or cardiology consult and monitoring
extended-release dipyridamole +
aspirin combination) If age <75 and PT/INR Consider contrast CT scan,
available, anticoagu- 4 vessel cerebral angio-
Control of risk factors lation with warfarin gram, MRA or CTA if
(target INR: 2-3) patient is:
Recommended vascular studies
such as carotid ultrasound to If age >75, warfarin 1) <45 years old,
document extracranial stenosis. (target INR: 2.0 [1.6-2.5]) 2) normotensive
If this reveals >70% stenosis, refer 3) has lobar ICH
to neurologist/neurosurgeon/ If anticoagulation is 4) uncertain cause of ICH
vascular surgeon for decision- contraindicated, give 5) suspected to have
making regarding CEA or stenting antiplatelets aneurysm, AV
(ASA 160-325 mg) malformation or
To document intracranial stenosis, vasculitis
recommend either TCD or MRA
or CTA.

­
Guidelines for Severe Stroke
Ascertain clinical diagnosis of stroke (history and physical exam are very important)
Management • Exclude common stroke mimickers
Priorities Basic emergent supportive care (ABCs of resuscitation)
Neuro-vital signs, BP, MAP, RR, temperature, pupils, oxygen saturation
Perform and monitor stroke scales (NIHSS, GCS)
Monitor and manage BP; treat if MAP >130
Provide O2 support to maintain O2 saturation >95%
• Precaution: Avoid precipitous drop in BP (not >15% of baseline MAP). Do not use rapid-
acting sublingual agents; when needed use easily titratable IV or oral antihypertensive
medication.
Identify comorbidities (cardiac disease, diabetes, liver disease, gastric ulcer, etc.)
Recognize and treat early signs and symptoms of increased ICP
Ensure adequate hydration. Recommended IVF-0.9% NaCl

Emergent • CBC with platelet count

Diagnostics • CBG or RBS
• PT/PTT
• Serum Na+ and K+
• ECG
• Non-contrast CT scan of brain or MRI-DWI as soon as possible
• If ICH, compute for hematoma volume

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Acute Stroke Treatment
Ischemic Hemorrhagic

Early Non-cardioembolic Supportive treatment:

Specific (Thrombotic, Lacunar) Cardioembolic 1. Mannitol 20%
Treatment 0.5-1 g/ kgBW
May give aspirin May give aspirin q 4-6 hours for 3-7 days
160-325 mg/day 160-325 mg/day
2. Neuroprotection
Refer to neuro specialist cases Refer to neuro specialist
of posterior circulation strokes cases of posterior 3. Give anticonvulsants for
within 12 hours of onset for circulation strokes clinical seizures and
CT-scan evaluation and decision regarding within 12 hours of proven subclinical or
confirmed thrombolytic therapy. onset for evaluation electrographic seizures.
and decision regarding Prophylactic AEDs are
Neuroprotection thrombolytic therapy generally not recom-
mended
Neuroprotection

If cerebellar infarct, consult If cerebellar infarct, Neurosurgery consult if:

neurosurgeon as soon as possible consult neurosurgeon 1. Patient not herniated;
as soon as possible Lobar bleed or located
Early supportive rehabilitation in putamen, pallidum,
Early supportive cerebellum;
rehabilitation
Family is willing to
accept consequences
of irreversible coma as
persistent vegetative
state
Goal is reduction of mortality

2. ICP monitoring is contem-

plated and salvage
surgery is considered

Early supportive
rehabilitation

Place of Intensive Care Unit

Treatment

Delayed Discuss prognosis with relatives of the patient in a most compassionate manner
Management
and Ischemic Hemorrhagic
Treatment
(Secondary Non-cardioembolic
Prevention) (Thrombotic, Lacunar) Cardioembolic

Antiplatelets (Aspirin, clopidogrel, Echocardiography and/ Long-term strict BP control
cilostazol, triflusal, dipyridamole, or cardiology consult and monitoring
extended-release dipyridamole +
aspirin combination) If age <75 and PT/INR Consider contrast CT scan,
available, anticoagula- 4 vessel cerebral angio-
Control of vascular risk factors tion with warfarin (target gram, MRA or CTA
INR: 2-3) if patient is:

If age >75, warfarin 1) <45 years old,

(target INR: 2.0 [1.6-2.5]) 2) normotensive
3) has lobar ICH
If anticoagulation is 4) uncertain cause of ICH
contraindicated, give 5) suspected to have
antiplatelets aneurysm, AV
(ASA 160 mg-325 mg) malformation or
vasculitis



 Acute Stroke Treatment
Early Specific Treatment for Ischemic Stroke

I. Antithrombotic Therapy in Acute Stroke

Drug Trial Design Result

International Stroke Trial 19,435 patients with acute Aspirin treated patients had
(IST, Lancet 1997; 349: ischemic stroke were slightly fewer deaths at 14 days,
1569-1581) randomized within 48 hrs to significantly fewer recurrent
Aspirin 300 mg day, subcuta- ischemic strokes at 14 days
neous heparin 5000 units BID and no excess of hemorrhagic
or 12,500 units BID, Aspirin strokes
plus heparin or neither
For patients receiving heparin,
there were fewer deaths or
recurrent strokes; however
Aspirin

there were more hemorrhagic

strokes & serious extracranial
hemorrhage, mostly in the
higher dose heparin group,
resulting in no net benefit.

Chinese Acute Stroke Trial 21,106 patients with acute Aspirin significantly reduced
(CAST, Lancet 1997;449: ischemic stroke within 48 hours the risk of recurrent stroke or
1641-1649) were randomized to Aspirin vascular death
160 mg OD or placebo for up
to 4 weeks

Fast assessment of Stroke 392 patients with TIA or minor The trial was prematurely
and Transient Ischemic Attack stroke within 24 hours were terminated because of failure
to Prevent Early Recurrence, randomized to Clopidogrel to recruit patients at the pre-
Clopidogrel-ASA vs Aspirin

(FASTER, Lancet Neurology (300 mg loading dose then specified recruitment rate
2007; 6:961-969) 75 mg/day plus Aspirin 81 mg because of increased use
or Aspirin 75 mg alone, with or of statins
without Simvastatin (in factorial
design) and followed up for Recurrent stroke at 90 days
90 days) were: Clopidogrel-ASA (7.1%),
Aspirin alone (10.1%),
absolute risk reduction of
3.8% p=0.19

Hemorrhagic events were

higher with the combination
treatment

Meta-analysis of randomized Ten trials involving 2885 The use of LMWH/heparinoids

controlled trials on low patients with acute ischemic was associated with significant
molecular weight heparins stroke reduction in venous thrombo-
LMWH

and heparins in acute ischemic embolism (DVT and PE).

stroke Low molecular weight heparin However, it had no significant
(Stroke 2000;31:31:1770-1778) or heparinoids given within effect on reducing death
7 days of stroke and disability at 6 months

II. Neuroprotection and Neuroprotect- acute stroke. Manage hypertension as per

ant Drugs recommendation.

A. NEUROPROTECTIVE INTERVENTIONS Avoid Hypoxemia

The 5 “H” Principle
AVOID hypotension, hypoxemia, hyperglycemia
or hypoglycemia and hyperthermia (fever) during
acute stroke in an effort to “salvage” the ischemic
penumbra.
Avoid Hypotension and allow Permissive Hyper-
tension during the 1st 7 days
• Aggressive BP lowering is detrimental in
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• Routine oxygenation in all stroke patients is
not warranted
• Maintain adequate tissue oxygenation (target
O2 saturation >95%)
• Do arterial blood gases (ABG) determination
or monitor oxygenation via pulse oximeter
• Give supplemental oxygen if there is evidence
of hypoxemia or desaturation
• Provide ventilatory support if upper airway is
threatened or sensorium is impaired or ICP
is increased.

Acute Stroke Treatment
Avoid Hypoglycemia or Hyperglycemia
Background: Hyperglycemia can increase
the severity of ischemic injury (causes lactic
acidosis, increases production of free radicals,
worsens cere­bral edema and weakens blood
vessels), whereas hypoglycemia can mimic a
stroke.
• Prompt determination of blood glucose should
be done in all stroke patients
• Ensure glycemic control at 110-180 mg/dL
preferably within the first 6 hours and main-
tain up to 3-5 days. May start intervention
with insulin if CBG >180 mg/dL
• Avoid glucose-containing (D5) IV fluids. Use
isotonic saline (0.9% NaCl)
Avoid Hyperthermia
Background: Fever in acute stroke is associated
with poor outcome possibly related to increased
metabolic demand, increased free radical
production and enhanced neurotransmitter
release.
Hyperthermia increases the relative risk of 1
year mortality by 3.4 times.
• For every 1oC increase in body tempera-
ture, the relative risk of death or disability
increased by 2.2
Hypothermia can reduce infarct size by 44% in
animal studies
• Search for the source of fever
• Treat fever with antipyretics and cooling
blankets
• Maintain normothermia.
B. NEUROPROTECTANT DRUGS:
Neuroprotectants are drugs with multi-modal
action:
• Protect against excitotoxins and help prolong
neuronal survival
• Block the release of glutamate and inflam-
matory cytokines, inhibit the formation of free
radicals and apoptosis
Bibliography:
Over 50 neuroprotective agents such as gluta-
mate, NMDA/AMPA antagonists, calcium channel
blockers, free radical scavengers have undergone
phase III clinical trials but most have failed. Several
reasons have been raised to explain the appar-
ent disappointments: animal models were wrong,
human trials were not done optimally (e.g., deter-
mination of time window, patient heterogeneity,
“targeted” neuroprotection which addresses single
mechanism of neuronal injury at a time, exclu-
sion of concomitant treatment with thrombolytic
agents).
Among the various pharmacologic agents inves-
tigated, CDP-choline (Citicoline) has shown great
promise as evidenced by numerous experimental
studies showing consistent improved functional out-
come and reduced infarct size in animal models of
stroke. Several trials in ischemic and hemorrhagic
strokes conducted worldwide have documented
its excellent safety profile. In individual patient
data pooling analysis (4 trials, 1652 patients) oral
citicoline given within the first 24 hours of moderate
to severe ischemic stroke significantly increased the
10
probability of global recovery by 30% at 3 months.
Similar positive result in reduction in death and
disability from acute ischemic stroke was obtained
in the latest meta-analysis in 2008.
CDP-choline has multimodal effects on the
ischemic and reperfusion cascade. It helps increase
phosphatidylcholine synthesis for membrane
stabilization and repair. It inhibits the activation of
phopholipase A2 and reduces oxygen free radicals
and inflammatory cytokines within the injured brain
during ischemia.
A randomized double-blind placebo controlled trial
on safety and efficacy of Citicoline 1 gm twice a day
in acute ischemic stroke within 24 hours for 6 weeks
known as International Citicoline on Acute Stroke
or ICTUS is currently underway to confirm results
of the pooled data analysis and meta-analysis.
The use of neuroprotectants in acute stroke
remains a matter of preference by the attend-
ing physician. The choice of Citicoline is a
reasonable option.
Two other pharmacologic agents with putative
neuroprotective properties are currently under-
going or recently completed phase III clinical
trials.
An international, multicenter double blinded,
placebo controlled randomized controlled trial on
Neuroaid known as Chinese Medicine Efficacy in
Stroke Recovery or CHIMES among patients with
acute ischemic stroke within 72 hours is currently
ongoing in several countries in Asia including Singa­
pore, Philippines, Thailand, Korea, Sri Lanka.
A double-blinded placebo controlled randomized
clinical trial to evaluate the safety and efficacy of
Cerebrolysin in patients with Acute Ischemic Stroke
in Asia in ASIA (CASTA) was recently completed
with results due this year.
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15. Labiche LA, Grotta JC. Clinical trials for cytoprotection in stroke.
NeuroRx 2004;1:46-70.
16. Lisberg P and Roine R. Hyperglycemia in Acute Stroke. Stroke 2004.
35:363-364.
17. Lizasoain I, Cardenas A, Hurtado O. et al. Targets of cytoprotection in
acute schemic stroke: present and future. Cerebrovasc Dis 2006: 21
(suppl 2)1-8.
18. Layden P, Wahlgren N. Mechanism of action of neuroprotectants in
stroke. Journal of stroke and cerebrovascular diseases. 2000; 9 (6):
9
19. Quin TJ and Lees KR. Hyperglycemia in acute stroke – to treat or not
to treat. Cerebrovasc Dis 2009; 27 suppl 1:148-155.
20. Secades J. and Lorenzo J. Citicoline: Pharmacological and clinical
review 2006 update: Methods and findings in experimental and clinical
pharmacology 2006:26 (suppl B): 1-56.
21. Venketasubramanian N, CL Chen, R. Gan, et al. on behalf of the
CHIMES Investigators, A double-blind, placebo-controlled, randomized,
multicenter study to investigate CHInese Medicine Neuroaid Efficacy
on Stroke recovery (CHIMES Study). International Journal of Stroke
2009;4:54-60
III. Anticoagulation In Acute Cardio­
embolic Stroke
A. Cardioembolic Sources
High Risk Low or Uncertain Risk
AF (valvular or Mitral valve Prolapse
non-valvular)
Rheumatic mitral Mitral annular calcification
stenosis
Prosthetic heart Patent foramen ovale
valves (PFO)
Recent MI Atrial septal aneurysm
LV/LA thrombus Calcific aortic stenosis
Atrial myxoma Mitral valve strands
Infective Endocarditis weight heparin in acute ischemic stroke. Stroke 2002;33:1927-1933.
Dilated cardiomyopathy anticoagulant treatment in acute cardioembolic stroke: A meta-analysis
Marantic endocarditis
Acute Stroke Treatment
C. When considering anticoagulation in acute
cardioembolic stroke, the benefits of anti­
coagulation in reducing early stroke recurrence
should be weighed against the risk of hemor-
rhagic transformation. The latter is higher in
patients with large infarction, severe strokes
or neurological deficits and uncontrolled hyper­
tension.
D. How to anticoagulate
1. Requirements for IV anticoagulation of patients
with cardiogenic source of embolism:
a. Heparin sodium in D5W
b. Infusion pump, if available
c. Activated partial thromboplastin time (aPTT)
or clotting time
2. Procedure:
a. Start intravenous infusion at 800 units
heparin/hour ideally using infusion pump. IV
heparin bolus is not recommended.
b. Perform aPTT as often as necessary, every 6
hours if needed, to keep aPTT at 1.5-2.5x the
control. Risk for major hemorrhage, including
intracranial bleed, progressively increases as
aPTT exceeds 80 seconds.
c. Infusion may be discontinued once oral
anticoagulation with warfarin has reached
therapeutic levels or once antiplatelet medica-
tion is started for secondary prevention.
To date, there has been no trial directly comparing effi­
cacy of unfractionated heparin vs LMWH in patients with
acute cardioembolic stroke. LMWH has the advantage
of ease of administration and does not require aPTT
monitoring.
Bibliography
1. Adams H. Emergent use of anticoagulation for treatment of patients with
ischemic stroke. Stroke 2002;33:856-861.
2. Hart R, Palacio S, Pearce L. Atrial fibrillation, stroke and acute
antithrombotic therapy. Stroke 2002;33:2722-2727.
3. Moonis, M, Fisher M. Considering the role of heparin and low-molecular
4. Paciaroni M, Agnelli G, Micheli S. et al. Efficacy and safety of
of randomized controlled trials. Stroke 2007; 38: 423-430.

B. Indications and contraindications for anticoagu-

lation in patients with Cardioembolic Stroke

Probably Indicated Contraindicated

Intracardiac thrombus Bleeding diathesis
Mechanical prosthetic Non-petechial intracranial
valve hemorrhage
Recent MI Recent major surgery
or trauma
CHF Infective endocarditis
Bridging measure for
long term anticoagu-
lation

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Acute Stroke Treatment
IV. ADIMINIsTRATION of rt-PA to ACUTE ISCHEMIC STROKE PATIENTS

Randomized Trials on Intravenous rt-PA Therapy in Acute Ischemic Stroke

Trial Design Results

NINDS tPA trial: National Institute 291 patients with acute ischemic No difference in neurologic
of Neurological Disorders and stroke <3 hours were randomized improvement at 24 hours, but
Stroke tPA trial (N Eng J Med to tpa (0.9 mg/kg IV) or placebo patients given IV rt-PA were
1995;333:1581 - 1587) and assessed for 4-point 30% more likely than controls to
improvement in NIH stroke scale have minimal or no disability at
or the resolution of neurological 3 months, despite more symp-
deficit within 24 hours; 333 tomatic ICH (6.4% vs 0.6%).
patients received IV rt-PA within Overall, there was no difference
3 hours of symptom onset and in mortality in 3 months.
were assessed for functional and
clinical outcome for 3 months

ECASS: European Australasian 620 patients with acute ischemic No difference in disability using
Cooperative Acute Stroke Study stroke <6 hours were randomized intention to treat analysis.
(JAMA 1995;274:1017-1025) to tPA 1.1 mg/kg or placebo However, there were 109 major
protocol violations. Post hoc
analysis excluding these patients
indicated better recovery for tPA
group at 90 days

ECASS II: Second European 800 patients with acute ischemic No significant difference was
Australasian Cooperative Acute stroke <6 hours were randomized seen in the rate of favorable
Stroke Study (Lancet 1998;352: to tPA 0.9 mg/kg or placebo outcome at 3 months between
1245-1251) rt-PA and placebo treated group

ATLANTIS A: Alteplase 142 patients with acute ischemic No significant difference was
Thrombolysis for Acute stroke <6 hours were randomized seen on any of the planned
Non-interventional Therapy in to tPA 0.9 mg/kg or placebo efficacy endpoints at 30 and
Ischemic Stroke 90 days between groups. The
(Stroke 2000;31:811-816) risk of symptomatic ICH was
increased with rt-PA treatment
particularly in patients treated
between 5 to 6 hours

ATLANTIS B: Alteplase 613 patients with acute ischemic No significant difference in

Thrombolysis for Acute stroke within 3-5 hours were functional recovery at 90 days
Non-interventional Therapy in randomized to tPA or placebo between groups. Risk of
Ischemic Stroke symptomatic intracerebral
(JAMA 1999;282:2019-2026) hemorrhage was increased
in tPA

EMS: Emergency Management 35 patients with acute ischemic IV/IA treatment resulted in
of Stroke Bridging Trial stroke <3 hours were randomized higher recanalization rate but
(Stroke 1999;30:2598-2605) to IV plus local intra-arterial (IA) no difference in outcome at 7
tPA vs intra-arterial tPA alone days or 3 months. The rate of
symptomatic intracerebral
hemorrhage was similar between
groups

ECASS III: European Australasian 821 patients with acute ischemic Significantly more patients in
Cooperative Acute Stroke Study stroke within 3 to 4.5 hours were the rt-PA treated group had
(N Eng J Med 2008; 359: randomized to tPA 0.9 mg/kg or favorable outcome at 3 months
1317-1329) placebo (52.4% vs 45.2%, p = 0.04). The
incidence of intracranial
hemorrhage was higher with
rt-PA but mortality did not
significantly differ between the
2 groups.

12

Administration of rt-PA to Acute Ischemic Stroke
Patients (0-3 hours)
1. Eligibility for IV treatment with rt-PA
• Age 18 or older.
• Clinical diagnosis of ischemic stroke causing a
measurable neurological deficit.
• Time of symptom onset well established to be less
than 180 minutes before treatment would begin.
2. Patient Selection: Contraindications and Warnings
• Evidence of intracranial hemorrhage on pretreat-
ment CT.
• Only minor or rapidly improving stroke symptoms.
• Clinical presentation suggestive of subarachnoid
hemorrhage, even with normal CT.
• Active internal bleeding.
• Known bleeding diathesis, including but not limited
to:
♦ Platelet count <100,000/mm
♦ Patient has received heparin within 48 hours and
has an elevated aPTT (greater than upper limit
of normal for laboratory)
♦ Current use of oral anticoagulants (e.g., war-
farin sodium) or recent use with an elevated
prothrombin time >15 seconds
• Patient has had major surgery or serious trauma
excluding head trauma in the previous 14 days.
• Within 3 months any intracranial surgery, serious
head trauma, or previous stroke.
• History of gastrointestinal or urinary tract hemor-
rhage within 21 days.
• Recent arterial puncture at a non-compressible
site.
• Recent lumbar puncture.
• On repeated measurements, systolic blood pres-
sure greater than 185 mm Hg or diastolic blood
pressure greater than 110 mm Hg at the time treat-
ment is to begin, and patient requires aggressive
treatment to reduce blood pressure to within these
limits.
• History of intracranial hemorrhage.
• Abnormal blood glucose (<50 or >400 mg/dL).
• Post myocardial infarction pericarditis.
• Patient was observed to have seizures at the
same time the onset of stroke symptoms were
observed.
• Known arteriovenous malformation, or aneurysm.
3. Treatment
• 0.9 mg/kg (maximum of 90 mg) infused over 60
minutes with 10% of the total dose administered
as an initial intravenous bolus over 1 minute.
4. Sequence of Events
• Draw blood for tests while preparations are made
to perform non-contract CT scan.
• Start recording blood pressure
• Neurological examination.
• CT scan without contrast.
• Determine if CT has evidence of hemorrhage.
• If patient has severe head or neck pain, or is som-
nolent or stuporous, be sure there is no evidence
of subarachnoid hemorrhage.
• If there is a significant abnormal lucency suggestive
of infarction, reconsider the patient’s history, since
the stroke may have occurred earlier.
• Review required test results — Hematocrit, Plate-
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Acute Stroke Treatment
lets, Blood glucose, PT or aPTT (in patients with
recent use of oral anticoagulants or heparin)
• Review patient selection criteria
• Infuse rt-PA.
• Give 0.9 mg/kg, 10% as a bolus, intravenously.
• Do not use the cardiac dose.
• Do not exceed the 90 mg maximum dose.
• Do not give aspirin, heparin or warfarin for 24
hours.
• Monitor the patient carefully, especially the blood
pressure. Follow the blood pressure algorithm (see
below and sample orders).
• Monitor neurological status.
5. Adjunctive Therapy
• No concomitant heparin, warfarin, or aspirin during
the first 24 hours after symptom onset. If heparin or
any other anticoagulant is indicated after 24 hours,
consider performing a non-contrast CT scan or
other sensitive diagnostic imaging method to rule
out any intracranial hemorrhage before starting an
anticoagulant.
6. Blood Pressure Control
Pretreatment
• Monitor blood pressure every 15 minutes. It should
be below 185/110 mm Hg.
• If over 185/110, BP may be treated with nitroglycerin
paste and/or one or two 10-20 mg doses of labetalol
given IV push or Nicardipine infusion of 5 mg/hour
titrate up by 2.5 mg every 5 - 15 mins interval. If
these measures do not reduce BP below 185/110
and keep it down, the patient should not be treated
with rt-PA.
During and after treatment.
• Monitor blood pressure for the first 24 hours after
starting treatment:
♦ Every 15 minutes for 2 hours after starting the
infusion, then
♦ Every 30 minutes for 6 hours, then
♦ Every hour for 18 hours.
• If systolic BP >230 mm Hg and/or diastolic BP is
121-140 mm Hg, give labetalol 20 mg intravenously
over 1 to 2 minutes. The dose may be repeated
and/or doubled every 10 minutes, up to 150 mg.
Alternatively either an intravenous infusion of 2 to 8
mg/min labetalol may be initiated after the first bolus
of labetalol or Nicardipine infusion 5 mg/hr infusion
is started and titrated up by 2.5 mg/hr every 5 - 15
mins interval until the desired BP is reached.
If satisfactory response is not obtained, use sodium
nitroprusside.
• If systolic BP is 180 to 230 mm Hg and/or diastolic
BP is 105 to 120 mm Hg on two readings 5 to 10
minutes apart, give labetalol 10 mg intravenously
over 1 to 2 minutes. The dose may be repeated
or doubled every 10 to 20 minutes, up to 150 mg.
Alternatively, following the first bolus of labetalol,
an intravenous infusion of 2 to 8 mg/min labetalol
may be initiated and continued until the desired
blood pressure is reached.
• Monitor blood pressure every 15 minutes during
the antihypertensive therapy. Observe for hypoten-
sion.
• If, in the clinical judgment of the treating physi-
13
Acute Stroke Treatment
cian, an intracranial hemorrhage is suspected, the
The search for a thrombolytic agent that can be
administration of rt-PA should be discontinued and
used beyond the 3 hours of acute ischemic stroke
an emergency CT scan or other diagnostic imaging
is being addressed by the ongoing DIAS-3 study or
method sensitive for the presence of intracranial
Desmoteplase In Acute Stroke Study. This double blind
hemorrhage should be obtained.
randomized trial will determine whether desmoteplase
is effective and safe in the treatment of patients with
Management of Intracranial Hemorrhage
acute ischaemic stroke when given within 3-9 hours
• Suspect the occurrence of intracranial hemorrhage
from onset of stroke symptoms. Patients should have
following the start of rt-PA infusion if there is any
an NIHSS Score of 4-24 and a documented vessel
acute neurological deterioration, new headache,
occlusion or high-grade stenosis on MRI or CTA in
acute hypertension, or nausea and vomiting.
proximal cerebral arteries. The Philippines is partici-
• If hemorrhage is suspected then do the following:
patory in this trial.
♦ Discontinue rt-PA infusion unless other causes
of neurological deterioration are apparent.
♦ Immediate CT scan or other diagnostic imaging
BLOOD PRESSURE MANAGEMENT
method sensitive for the presence of hemor-
AFTER ACUTE STROKE
rhage.
♦ Draw blood for PT, aPTT, platelet count, fibrino-
A. BP management in Acute Ischemic Stroke
gen, and type and cross (may wait to do actual
type and cross).
1. Use the following definitions:
♦ Prepare for administration of 6 to 8 units of
cryoprecipitate containing factor VIII.
Cerebral Perfusion Pressure (CPP) = MAP-ICP
♦ Prepare for administration of 6 to 8 units of
MAP = 2 (diastolic) + systolic
platelets.
3
• If intracranial hemorrhage is present:
Normal CPP = 70-100 mmHG
♦ Obtain fibrinogen results.
Normal ICP = 5-10 mmHG
♦ Consider administering cryoprecipitate or plate-
lets if needed.
2. Check if patient is in any condition that may increase
♦ Consider alerting and consulting a hematologist
BP such as pain, stress, bladder distention or
or neurosurgeon.
constipation, which should be addressed accord-
♦ Consider decision regarding further medical
ingly.
and/or surgical therapy.
♦ Consider second CT to assess progression of
3. Allow “permissive hypertension” during the first
intracranial hemorrhage.
week to ensure adequate CPP but ascertain cardiac
♦ A plan for access to emergent neurosurgical
and renal protection.
consultation is highly recommended.

This Protocol is Based on Research Supported by the National Institute a. Treat if SBP>220 or DBP>120 or MAP>130
of Neurological Disorders and Stroke (NINDS) (NOI-NS-02382, N01-NS-
02374, NO1-NS-02377, NO1-NS-02381, NO1-NS-02379, NOi-NS-02373, b. Defer emergency BP therapy if MAP is within
NO1-NS-02378, NOl-NS-02376, NOl-NS-02380).
110-130 or SBP=185-220 mmHg or DBP=l05-
120 mmHg, unless in the presence of:
Expansion of IV rt-PA Treatment Time Window up ♦ Acute MI
to 4.5 Hours ♦ Congestive heart failure
♦ Aortic dissection
Eligibility for IV treatment follows the same criteria as ♦ Acute pulmonary edema
treatment within the first 3 hours with the following addi­ ♦ Acute renal failure
tional exclusion criteria: ♦ Hypertensive encephalopathy
• Patients older than 80 years old
• Patients on oral anticoagulants, regardless of INR Rationale for Permissive Hypertension:
level • In acute ischemic stroke, autoregulation
• Patients with NIHSS >25 is paralyzed in the affected tissues with
• Patients with stroke and diabetes CBF passively following MAP. Rapid BP
lowering can lead to further ↓ perfusion in
Ancillary care for patients receiving IV rt-PA treatment the penumbra.
at 3 - 4.5 hours after acute ischemic stroke is similar to • HPN is typically present in acute stroke,
that listed above. with spontaneous decline within the first 5-7
Bibiography
days.
• ↑ ICP during the acute phase of large infarcts
1. Adams H, del Zoppo G, Alberts M et aL Guidelines for the early reduces the net CPP.
management of patients with ischemic stroke. 2007 Guidelines update, • Several reports have documented neurologi-
a scientific statement from the Stroke Council of the American Heart
Association. Stroke 2007;38:1655- 1711. cal deterioration & poor outcome from rapid
2. Del Zoppo, G, Saver J,Juach E and Adams, H on behalf of the American and aggressive pharmacologic lowering of
Heart Association Stroke Council. Expansion of the Time Window for BP.
Treatment of Acute Ischemic Stroke with Tissue Plasminogen Activator, a
science advisory from the American Heart Association / American Stroke
Association. Stroke 2009; 40:2945—2948.
4. Use the following locally available intravenous anti-
hypertensives in acute stroke to achieve target MAP
= 110-130 mmHg:
14
 Acute Stroke Treatment
Drug Dose Onset of Duration Availability/ Stability Adverse Action
Action of Action Dilution Reactions

1-15 mg/hour 5-10 mins 1-4 hours (10 mg/10 mL 1 to 4 hours Tachycardia, Inhibits calcium
amp); 10 mg headache, ion from
in 90 mL flushing entering slow
NSS/D5W dizziness, channel,
Nicardipine

somnolence, producing
nausea coronary,
vascular,
smooth
muscle relax-
ation &
vasodilation

IV push 10-20 10-20 mins 3-8 hours 25 mg/mL 4 days Tachycardia, Direct vasodila-
Hydralazine

mg/dose q 4-6 amp; 25 flushing tion of arterioles

hours as mg/tab headache, & decreased
needed, may vomiting, systemic
increase to 40 increased resistance
mg/dose angina

5 mg lV push 2-5 mins 2-4 hours 5 mg/mL in 72 hours Orthostatic Alpha- & beta
over 2 mins 40 mL vial; hypotension, blocker. Beta-
repeat with 250 mg in drowsiness, adrenergic
incremental 250 mL dizziness, blocking activity
dose of 10, 20, NSS/D5W lightheaded- is 7x > than
Lobetalol

40, 80 mg until ness, alpha-adrener-

desired BP is dyspnea, gic blockers.
achieved or a wheezing, Produces dose-
total dose of & broncho- dependent ↓
300 mg has spasm in BP without
been adminis- significant ↓ in
tered HR or cardiac
output

0.25-0.5 mg/ 2-10 mins 10-30 mins 100 mg/ 48 hours Hypotension, Short-acting
kg IV push 10 mL vial; bradycardia, beta-adrenergic
1-2 mins 2500 mg in AV block, blocking agent.
followed by 250 mL agitation, At low doses,
infusion of 0.05 D5W/NSS confusion, has little effect
mg/kg/min wheezing/ on beta 2
broncho- receptors
Esmolol

If there is no constriction, of bronchial &

response, phlebitis vascular smooth
repeat 0.5 muscle
mg/kg bolus
dose & ↑ infu-
sion to 0.10 mg/
kg/min. maxi-
mum infusion
rate=0.30 mg/
kg/min

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Acute Stroke Treatment
5. Treat patients who are potential candidates for rt-PA
therapy who have persistent elevations In SBP >185
mmHg or DBP >110 mmHg with small doses of IV
antihypertensive agents. Maintain BP just below these
limits.
B. Blood pressure management in Acute Hyperten-
sive ICH
Treat if SBP >180 mmHg or MAP >130 mmHg.
Maintain MAP = 110 or SBP = 160 mmHg
• Absence of ischemic penumbra allows for more
aggressive BP management
• Sustained hypertension may promote early hema­
toma expansion and worse, edema
• Hypotension may result in cerebral hypoperfusion
especially in the setting of increased intracranial
pressure (ICP)
• Two recent phase II clinical trials on BP lowering
namely ATACH and INTERACT has shown that
intensive BP lowering to SBP = 140 in acute ICH
is feasible and is probably safe. Phase III clinical
studies are ongoing to determine its clinical
efficacy.
Bibliography
1. Adams H, Adams R, del Zoppo G, Goldstein L. Guidelines for the early
management of patients with ischemic stroke. 2005 Guidelines update,
a scientific statement from the Stroke Council of the American Heart
Association. Stroke 2005;36:916-923.
2. Broderick JP, Adams HP, Barsan W, et al. Guidelines for the management
of spontaneous intracerebral hemorrhage: a statement for healthcare
professionals from a special writing group of the Stroke Council of the
American Heart Association. Stroke 1999;30:905-915.
3. Fogelhoim R, Avikainen S and Murros K. Prognostic value and
determinants of first day mean arterial pressure in spontaneous
supratentorial intracerebral hemorrhage. Stroke 1997;28:1396-1400.
4. Guyton A and HaII J. Guyton and Hall’s Textbook of Medical Physiology,
11th ed. USA: WB Saunders; 2005.
5. Kidwell CS, Saver JL, Mattiello J, et al. Diffusion perfusion MR evaluation
of perihematomal injury in hyperacute intracebral hemorrhage. Neurology
2001;57:161 1-1617.
6. Powers WJ, Zazulia AR, Videen TO, et al. Autoregulation of cerebral
blood flow surrounding acute (6-22hours) intracerebral hemorrhage.
Neurology 2001;57:18-24.
7. Qureshi A, Wilson D, Hanley D, Traystman R. No evidence for an
ischemic penumbra in massive experimental intracerebral hemorrhage.
Neurology I 999;52:266-272.
8. Schellinger P, Fiebach J, Hoffman K, et al. Stroke MRI in intracerebral
hemorrhage: is there a perihemorrhagic penumbra? Stroke 2003;34:1647-
1680.
9. The Brain Matters Stroke Initiative. Acute Stroke Management Workshop
Syllabus. Basic Principles of Modern Management for Acute Stroke.
16
MANAGEMENT OF INCREASED INTRACRANIAL
PRESSURE
A. Signs and symptoms of increased ICP
1. Deteriorating level of sensorium
2. Cushing's triad
i. Hypertension
ii. Bradycardia
iii. Irregular respiration
3. Anisocoria
B. Management options for increased ICP
General:
1. Control agitation and pain with short-acting medica-
tions, such as NSAIDS and opioids.
2. Treat fever aggressively. Avoid hyperthermia.
3. Control seizures if present. May treat with phenytoin
with a loading dose of 18-20 mg/kg IV then main-
tained at 3-5 mg/kg or Levetiracetam 500 mg/IV q 12.
Status epilepticus should be managed accordingly.
4. Strict glucose control between 110-180 mg/dL.
5. Maintain normal fluid and electrolyte balance.
a. Avoid excessive free water or any hypotonic
fluids such as D5W. Potential sources of free
water including hypotonic tube feedings, medi-
cations mixed in D5W, nasogastric tube flushes
with water should be minimized.
b. Maintain normal volume status (i.e., 3-3.5 liters
per day in a 60 kg patient).
c. Encourage hyperosmolar state with hypertonic
saline and/or induce free water clearance with
mannitol or diuretics.
6. Use stool softeners to prevent straining.
Specific:
1. Elevate the head at 30 to 45 degrees to assist
venous drainage.
2. Do CSF drainage in the setting of hydrocephalus.
3. Administer osmotic therapy:
• Give Mannitol 20%. Typical doses range from
0.5-1.5 g/kg every 3-6 hours. Doses up to 1.5
g/kg are appropriate when treating a deterio­-
rating patient because of mass effect.
• Hypertonic Saline is an option. It has the advan-
tage of maintaining an effective serum gradient
or rise in osmolality for sustained periods with
lower incidence of intracranial hypertension.
• Always maintain serum osmolality at 300-320
mOsmol/kg
Serum osmolality = 2 (Na) + glucose/18 + BUN/2.8
4. Hyperventilate only in impending herniation by
adjusting tidal volume to achieve target PCO2 levels
30-35 mm Hg. Hyperventilation is recommended
only for a short term as its effect on CBF and ICP is
short lived (≅ 6 hours). Prophylactic hyperventilation
without regard to the level of ICP and the clinical
state should not be done.
5. Carefully intubate patients with respiratory failure
defined as SpO2 of less than 90% by pulse oximeter
and PaO2 <60 mmHg, and/or PaCO2 >55 mmHg
by arterial blood gas analysis.
6. Consider surgical evacuation or decompressive
hemicraniectomy if indicated.
7. ICP catheter insertion is useful for the diagnosis,
monitoring and therapeutic lowering of increased
ICP. It is recommended in patients with a GCS ≤8,
those with significant IVH or hydrocephalus. CPP
should be maintained at 60-70 mmHg.
 Acute Stroke Treatment
C. Sedatives and Narcotics available locally

Drugs Usual Dose Onset of Duration Comments Availablity/

Action of Effect Duration

Midazolam 0.025-0.35 1 to 5 min 2 hours Unpredictable sedation 15 mg/3 mL amp;

mg/kg 5 mg/5 mL amp;
50 mg in 100 mL
NSS/D5W
Diazepam 0.1-0.2 mg/kg Immediate 20 to 30 Sedation can be reversed 10 mg/2 mL amp;
minutes with flumazenil (0.2-1 mg 50 mg in 250 mL
at 0.2 mg/min at 20 min NSS/D5W
interval, max dose 3 mg
in one hour)
Propofol 5-50 ug/kg/min <40 secs 10 to 15 min Expensive (10 mg/mL)
100 mL vial
(premixed)
Ketorolac 50-100 mg 1V 1 hour 6 to 8 hours NSAID 30 mg/mL amp
Tramadol 50-100 mg 1V 1 hour 9 hours Centrally acting synthetic 50 mg/2 mL amp;
analgesic compound not 100 mg/2 mL amp
chemically related to
opiates but thought to bind
to opioid receptors and inhibit
reuptake of NE and serotonin
Fentanyl 50-100 ug/hour 1-2 mins >60 min Can be easily reversed 100 ug/2 mL;
with naloxone (0.4-2 mg IVP; 2,500 ug in 250 mL
repeat at 2-3 min intervals, NSS/D5W
max dose 10 mg)* 110x more
potent than morphine
Morphine 2-5 mg/hour 5 mins >60 min Opioid 10 mg/mL gr 1/6;
16 mg/mL gr 1/4
Dexme- 1 mcg/kg/hr LD 30-60 secs 3-5 mins 200 mcg/2 mL vial
detomidine for 10 mins then
(Precedex) maintenance
dosing at 0.4 mcg/
kg/hr (Dose range:
0.2-0.7 mcg/hr)

STROKE SCALES II. National Institutes of Health (NIH) Stroke Scale

I. Glasgow Coma Scale
Category Score
Eye Opening
Spontaneous 4
To speech 3
To pain 2 (not stereotyped)
None 1
Best Motor Response
Obeys 6
Localizes 5
Withdraws 4
Abnormal flexion
(decorticate) 3 Commands 1 = Performs one task correctly
Abnormal extension
(decerebrate) 2
None 1
Best Verbal Response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1 1 = Partial hemianopia
Items Scale Definition
Ia. Level of 0 = Alert, keenly responsive
Consciousness 1 = Not alert, but arousable by
(LOC) minor stimulation to obey, answer
or respond
2 = Not alert, requires repeated
stimulation to attend, or is obtund-
ed and requires strong or painful
stimulation to make movements
3 = Responds only with reflex mo-
tor or autonomic effects or totally
unresponsive, flaccid, areflexic
Ib. LOC Questions 0 = Answers to both questions cor-
rectly
1 = Answers one question correctly
2 = Answers neither question correctly
Ic. LOC 0 = Performs both tasks correctly
2 = Performs neither task correctly
2. Best gaze 0 = Normal
1 = Partial gaze palsy. Gaze is
abnormal in one or both eyes but
forced deviation or total gaze pare-
sis is not present.
2 = Forced deviation, or total gaze
paresis is not overcome by oculo-
cephalic maneuver
3. Visual 0 = No visual loss

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Acute Stroke Treatment
Items Scale Definition Items Scale Definition

2 = Complete hemianopia can be exchanged is limited; listener

3 = Bilateral hemianopia (blind, carries the burden of communication
including cortical blindness) 3 = Mute, global aphasia; no usa­ble
speech or auditory comprehension
4. Facial palsy 0 = Normal symmetrical movement
1 = Minor paralysis (flattened naso­ 10. Dysarthia 0 = Normal
labial fold, asymmetry on smiling) (Fig. 2) 1 = Mild to moderate; patient slurs at
least some words and at worst, can
5. Motor (Arm) be understood with some difficulty
5a. Leftarm 2 = Severe; patient’s speech is so
5b. Right arm 0 = No drift; limb holds 90 (or 45) slurred as to be unintelligible in the
degrees for full 10 seconds absence of or out of proportion to
1 = Drifts; limb holds 90 (or 45) any dysphasia, or is mute/anarthric
degrees but drifts down before 9 = intubated or other physical
full 10 seconds; does not hit bed barrier; explain
or other support 11. Extinction & 0 = No abnormality
2 = Some effort against gravity, Inattention 1 = Visual, tactile, auditory, spatial
limb cannot get up to or maintain or personal inattention or extinct­ion
(if cued) 90 (or 45) degrees; drifts to bilateral simultaneous stimula-
down to bed, but has some effort tion in one of the sensory modalities
against gravity 2 = Profound hemi-attention or hemi-
3 = No effort against gravity, limb falls inattention to more than one modal-
4 = No movement ity. Does not recognize own hand or
9 = Amputation or joint fusion; explain orients to only one side of space.
6. Motor (Leg)
6a. Right leg 0 = No drift; leg holds 30-degree *Total score = 42
6b. Left leg position for full 5 seconds
1 = Drifts; leg falls by the end of the 5-
second period but does not hit bed Fig. 1: Aphasia
2 = Some effort against gravity,
leg falls to bed by 5 seconds but Ask the patient to describe what is happening on the
has some effort against gravity picture and name items.
3 = No effort against gravity, leg
falls to bed immediately
4 = No movement
9 = Amputation or joint fission; explain
7. Limb ataxia 0 = absent
1 = Present in one limb
2 = Present in two limbs
9 = Amputation or joint fusion; explain
8. Sensory 0 = Normal; no sensory loss
1 = Mild to moderate sensory loss;
patient feels pinprick is less sharp Fig. 2: Dysarthria
or dull on the affected side; or
there is a loss of superficial pain Ask the patient to read or repeat words from the list.
with pinprick, but patient is aware
he/she is being touched MAMA
2 = Severe or total sensory loss; TIP-TOP
patient is not aware of being FIFTY-FIFTY
touched in the face, arm or leg THANKS
HUCKLEBERRY
9. Best Language 0 = No aphasia
BASEBALL PLAYER
(Fig. 1) 1 = Mild to moderate aphasia; some
obvious loss of fluency or facility
of comprehension, without signifi-
cant limitation on ideas expressed
or form of expression. Reduction
of speech and/or comprehension,
however, makes conversation on
provided material difficult.
2 = Severe aphasia; all communi-
cation is through fragmentary ex-
pression; great need for inference,
questioning and guessing by the
listener. Range of information that

18
 Acute Stroke Treatment
III. Modified Rankin Scale
Score
No symptoms at all 0
No significant disability despite 1
symptoms; able to carry out all usual
duties and activities
Slight disability; unable to carry out all 2
previous activities but able to look after
own affairs without assistance
Moderate disability; requiring some 3
help but able to walk without assistance
Moderately severe disability; unable to 4
walk without assistance and unable to attend
to own bodily needs without assistance
Severe disability; bedridden, incontinent and 5
requiring constant nursing care and attention
Death 6
Bibliography
1. Brott T, Adams H, Olinger CP, et al. Measurements of acute cerebral
infarction: a clinical examination scale. Stroke 1989;20:864-870.
2. Goldstein LB, Bartels C. Davis JN. Interrater reliability of the NIH Stroke
Scale. Arch Neurol 1989;46:660-662.
3. Rankin J. Cerebral vascular accidents in patients over the age of 60.
Scot Med J 1957;2:200- 215.
4. Van Swieten JC, Koudstaal JP, Visser MC, et al. Interobserver agreement
for the assessment of handicap in stroke patients. Stroke 1988;19:604-607.
5. The Brain Matters Stroke Initiative. Acute Stroke Management Workshop
Syllabus. Basic Principles of Modern Management for Acute Stroke.

Learn to access drug info on your cellphone. Send PPD to 2600 for Globe/Smart/Sun users. 19
Acute Stroke Treatment
Index of Drugs Mentioned in the Guideline
This index is not part of the guideline. It lists the products and/or their therapeutic classes as mentioned in the guideline. For
the doctor's convenience, brands available in the PPD references are listed under each of the classes. For drug information,
refer to the PPD references (PPD, PPD Pocket Version, PPD Text, PPD Tabs, and www.TheFilipinoDoctor.com).

Anticoagulants Citilin
Citxl
Heparin Sodium Neuropro
Heparin Leo Nicholin
Somazine
Antiplatelets Zyndes

Aspirin Hypnotic /Sedative

Aspilets
Aspilets-EC Benzodiazepines
Bayer Aspirin 100 mg
Bayprin EC Diazepam
Cor-30 Trankil
Cortal Valium
Rhea Aspirin Midazolam
Aspirin + Clopidogrel Dormicum
Norplat-S Hypozam
Aspirin + Dipyridamole Sedoz
Aggrenox
Cilostazol General Anesthetics
Ciletin
Clazol Parenteral
Pencil 50/100 Propofol
Platecil Fresofol MCT/LCT 1%
Pletaal IV-Pro
Trombocil Neorof
Clopidogrel Spiva with MCT-LCT
Actaclo
Cardogrel Analgesic/Antipyretics & Muscle
Clopimax Relaxants
Clopimet
Clopivaz NSAIDS
Cloplat Ketorolac
Cloprez Acular
Clotiz Ketodol
Deplatt Ketomed
Dorell Kortezor
Klopide Oradol
Noklot Toradol
Norplat Xevolac
Pharex Clopidogrel
Platec Opiates & Antagonist
Platelex Fentanyl
Plavix Durogesic D Trans
Plogrel Sublimaze
RiteMED Clopidogrel Morphine
Thromvix Hizon Morphine Sulfate
Vivelon MST Continus
Winthrop Clopidogrel Tramadol
Dipyridamole Dolmal
Persantin Radol
Ticlopidine HCl Siverol
TDL
Calcium Antagonist Tramal
Vistra
Nicardipine HCl Vitral
Cardepine Tramadol + Paracetamol
Algesia
Vasodilators Cetra
Dolcet/Dolcet Mini
Hydralazine HCl Nodolor P
P-Dol
CNS Stimulants/Neurotonics Supercet

Citicoline
Brainact
Cholinerv

20