Non-Hemorrhagic Stroke Latest

NON-HEMORRHAGIC
STROKE
GUIDELINES FOR TREATMENT
(Stroke Society of the Philippines Handbook, 6
th
ed)
OBJECTIVE

To present the guidelines for treatment of Acute Stroke and Transient
Ischemic Attack (TIA)
To discuss briefly the guidelines for Antiplatelet Therapy in
Noncardioembolic Stroke or Transient Ischemic Attack (TIA)
Outline
Stroke Scales (Glasgow Coma Scale, NIHSS)
Classification of Acute Stroke Based on Clinical Severity
Guidelines for Management of TIA, Mild -, Moderate -, and Severe Stroke
Early Specific Treatment of Ischemic Stroke
Management of Increased Intracranial Pressure
Guidelines for Antiplatelet Therapy in Noncardioembolic Stroke or
Transient Ischemic Attack (TIA)

GLASGOW COMA SCALE
National Institute of Health
Stroke Scale
CLASSIFICATION OF
ACUTE STROKE
BASED ON
CLINICAL SEVERITY
TRANSIENT ISCHEMIC ATTACK (TIA)
a transient episode of neurological dysfunction caused by focal brain, spinal,
or retinal ischemia, without evidence of acute infarction in which clinical symptoms
typically last less than an hour
MILD STROKE
Alert patients with any (or combination) of the ff:
Mild pure motor weakness of one side of the body
Pure sensory deficit
Slurred but intelligible speech
Vertigo with incoordination
Visual field defects alone
or NIHSS score: 0-5
MODERATE STROKE
Awake patient with significant motor and/or sensory and/or language
and/or visual deficit
or
Disoriented, drowsy or light stupor with purposeful response to painful
stimuli
or
NIHSS score: 6-21
SEVERE STROKE
Deep stupor or comatose patient with non-purposeful response, decorticate
or decerebrate posturing to painful stimuli
or
Comatose patient with no response to painful stimuli
or
NIHSS score: >22
Recommended Place of Treatment
(TIA)
OPD
Occurred >2 wks prior (work-up
should be done within 24-48hrs)
ASU
w/in 48hrs
Crescendo TIAs (multiple & increasing
symptoms)
With known high-risk cardiac source of
embolism
Known hypercoagulable state or
symptomatic ICA stenosis
ABCD
2
score >3
High Risk

AF (valvular or non-valvular)
Rheumatic MS
Prosthetic heart valves
Recent MI
LV/LA thrombus
Atrial myxoma
Infective endocarditis
Dilated cardiomyopathy
Marantic endocarditis

a risk assessment tool designed to
improve the prediction of short-term
stroke risk after a transient ischemic
attack (TIA)
to predict the risk of stroke within 2
days after a TIA, but also predicts
stroke risk within 90 days
Higher ABCD
2
scores are associated
with greater risk of stroke during the
2, 7, 30, and 90 days after a TIA
Mild Stroke
ASU/ regular room

Moderate Stroke
ASU/ ICU

Severe Stroke
ICU
Recommended Place of Treatment
GUIDELINES
Management Priorities
Emergent Diagnostics
Early Specific Treatment
Delayed Management and Secondary Prevention
GUIDELINES FOR THE
MANAGEMENT OF
TRANSIENT ISCHEMIC ATTACK
(TIA)
Transient Ischemic Attack
Ascertain clinical dx of TIA
Exclude common TIA mimics
ID comorbidities
ABCs of resuscitation
Monitor the ff:
NVS, pupil size, BP, MAP, RR, temp, SO
2

Perform stroke scales (NIHSS, GCS) and risk
stratification using ABCD
2
scale

Treat BP if MAP >130
Avoid precipitous drop (not >15% of baseline MAP) within
24 hrs
Do not use rapid-acting SL agents; when needed, use easily
titratable IV or short-acting oral antihypertensive meds
Ensure appropriate hydration
0.9% NaCl
CBC
CBG or RBS
PT, aPTT
ECG
Cranial MRI-DWI is preferred; may do
NCCT scan if MRI is not available/
possible



Cardioembolism NOT suspected
ASA 160-325 mg/day as early as
possible & continue for 14 days
ASA 80mg + Clopidogrel 75mg
may be considered for short-term
treatment
Ensure neuroprotection*
Cardioembolism Suspected
IV heparin or SQ LMWH for
individuals at high risk of early
recurrence (AF with thrombus, VHD,
or MI) or ASA 160-325mg/day (if
anticoagulation is not possible or is
contraindicated)
If IE is suspected, give antibiotics and
DO NOT anticoagulate


Give antiplatelets (ASA,
clopidogrel, cilostazol, triflusal,
dipyridamole + ASA)
Control/treat risk factors
Carotid UTZ (extracranial stenosis)
TCD studies or CTA/MRA
(intracranial stenosis)
Echocardiography and/or refer to
cardiologist
NOACs > dose-adjusted warfarin
ASA 160-325mg/day if
anticoagulation is contraindicated
ASA + Clopidogrel is reasonable


Screening for hypercoagulable states and drug/toxicology tests may be
considered for young patients with TIA/stroke especially when no vascular
risk factors exist and no underlying cause is identified.
If vasculitis is suspected, may do ESR, ANA and lupus anticoagulant tests
TEE to rule out PFO in cryptogenic strokes
GUIDELINES FOR THE
MANAGEMENT OF
MILD STROKE
Mild Stroke
Ascertain clinical dx of stroke
Exclude common stroke mimics
ID comorbidities
Monitor the ff:
2

Perform and monitor stroke scales
(NIHSS, GCS)

Provide O
2
support to maintain SO
2
>94%
24 hrs
0.9% NaCl
CBC
CBG or RBS
PT, aPTT
ECG
Cranial NCCT scan or MRI-DWI as soon as
possible
If ICH is evident, compute for the hematoma
volume

Mild Stroke

Mild Stroke
(requires neuroimaging confirmation)
ISCHEMIC

ASA 160-325mg/day as early as possible
and continue for 14 days
ASA 80mg + Clopidogrel 75mg may
considered for short-term treatment
Consider IV heparin or SQ LMWH for
individuals at high risk of early recurrence
(AF with thrombus, VHD, or MI) or ASA
160-325mg/day (if anticoagulation is not
possible or is contraindicated)
If IE is suspected, give antibiotics and DO
NOT anticoagulate

(Thrombotic, Lacunar)

Mild Stroke
HEMORRHAGIC

Early neurology and/or neurosurgery consult for all ICH cases
Monitor and maintain target SBP 140mmHg during the first week
Early rehabilitation once stable within 72hrs
Give AEDs for clinical seizures and proven subclinical or electrographic seizures
Prophylactic AEDs and steroids are generally not recommended.
Monitor/ correct for metabolic parameters and coagulation/ bleeding abnormalities
Follow recommendations for neurosurgical intervention

Mild Stroke
ISCHEMIC

Give antiplatelets (ASA, clopidogrel,
cilostazol, triflusal, dipyridamole, ER-
dipyridamole + ASA)
TCD studies or CTA/MRA (intracranial
stenosis)
cardiologist
ASA 160-325mg/day if anticoagulation is
contraindicated

Mild Stroke
HEMORRHAGIC

Long-term strict BP control and monitoring
Contrast CT scan, 4-vessel cerebral angiogram, MRA or CTA if the patient
is:
<45 y/o
Normotensive
Has lobar ICH
Has uncertain cause of ICH
Suspected to have aneurysm, AVM, or vasculitis
GUIDELINES FOR THE
MANAGEMENT OF
MODERATE STROKE
Moderate Stroke
ID comorbidities
Monitor the ff:
2

Perform and monitor stroke scales (NIHSS,
GCS)

Provide O
2
2
>94%
24 hrs
Recognize and treat for early S/Sx of
increased ICP
0.9% NaCl
CBC
CBG or RBS
PT, aPTT
Serum Na+ and K+
ECG
possible
If ICH is evident, compute for the hematoma volume

Moderate Stroke

Moderate Stroke
ISCHEMIC

Refer to neurologist for evaluation and
decision
w/in 3-4.5hrs of stroke onset:
IV thrombolysis (rt-PA)
w/in 6hrs:
Intra-arterial thrombolysis (in specialized
centers)

ASA 160-325mg/day 24 hrs after IV rt-PA
treatment and continue for 14 days
Early rehabilitation once stable within 72
hrs

Moderate Stroke
ISCHEMIC

decision
w/in 6hrs:
centers)
If px is ineligible for thrombolytic therapy,
or 24hrs post-rt-PA treatment:
IV heparin or SQ LMWH for individuals at
high risk of early recurrence; or
not possible or is contraindicated
if IE is suspected, give antibiotics and DO
NOT anticoagulate
Early rehabilitation once stable within 72 hrs

Moderate Stroke
HEMORRHAGIC

Early neurology and/or neurosurgery consult for all ICH cases
Monitor and maintain target SBP 140mmHg during the first week
Early rehabilitation once stable within 72hrs
Monitor/ correct for metabolic parameters and coagulation/ bleeding abnormalities
Follow recommendations for neurosurgical intervention

Moderate Stroke
ISCHEMIC

dipyridamole + ASA)
cardiologist
contraindicated

Moderate Stroke
HEMORRHAGIC

is:
<45 y/o
Normotensive
Has lobar ICH
GUIDELINES FOR THE
MANAGEMENT OF
SEVERE STROKE
Severe Stroke
ID comorbidities
Monitor the ff:
2

Perform and monitor stroke scales (NIHSS,
GCS)

Provide O
2
2
>94%
24 hrs
Recognize and treat for early S/Sx of
increased ICP
0.9% NaCl
CBC
CBG or RBS
PT, aPTT
Serum Na+ and K+
ECG
possible
If ICH is evident, compute for the hematoma volume

Severe Stroke

Severe Stroke
ISCHEMIC

decision
w/in 6hrs:
centers)

ASA 160-325mg/day 24 hrs after IV rt-PA
treatment and continue for 14 days
Early rehabilitation once stable within 72
hrs

Severe Stroke
ISCHEMIC


May give ASA 160-325mg/day
Refer to a neurologist for cases of
posterior circulation strokes within 12 hrs
of onset for evaluation and decision
regarding thrombolytic therapy

For cases of cerebellar infarct, refer to a
neurosurgeon as soon as possible
Early supportive rehabilitation

Severe Stroke
HEMORRHAGIC

Supportive treatment: Mannitol 20% 0.5-1g/kg BW q 4-6h for 3-7days

Severe Stroke
HEMORRHAGIC

Neurosurgical consult if:
Px is not herniated
Location of bleed is lobar, putamen, pallidum, or cerebellum
Pxs family is willing to accept consequences of irreversible coma or persistent vegetative state
ICP monitoring is contemplated and salvage surgery is considered

Early supportive rehabilitation
GOAL IS REDUCTION OF MORTALITY

Severe Stroke
ISCHEMIC

dipyridamole + ASA)
cardiologist
contraindicated

Severe Stroke
HEMORRHAGIC

is:
<45 y/o
Normotensive
Has lobar ICH
Discuss the prognosis of the patient with family/ relatives in
the most compassionate manner.
EARLY SPECIFIC TREATMENT OF
ISCHEMIC STROKE
ANTITHROMBOTIC THERAPY
IN ACUTE STROKE
Aspirin (ASA)
[Clopidogrel + ASA] vs ASA alone
Clopidogrel ASA vs ASA alone
Cilostazol vs ASA
LMWH
NEUROPROTECTION
The Five H Principle:

AVOID
Hypotension, Hypoxemia, Hyperglycemia, Hypoglycemia and Hyperthermia

during acute stroke in an effort to salvage the ischemic penumbra.
Neuroprotective Interventions
1. Avoid HYPOTENSION and allow permissive hypertension during
the first (7) days.

Mean Arterial Pressure (MAP) = 2 (DBP) + SBP
3

Cerebral Perfusion Pressure (CPP) = MAP - ICP
Check if Px has any condition that may increase BP and address accordingly.
Treat if SBP >220 mmHg or DBP >120 mmHg, or MAP >130.
Defer E BP therapy if MAP is within 110-130, or SBP = 185-220mmHg
or DBP = 105-120mmHg, UNLESS:
Px is a candidate for thrombolytic therapy
Presence of AMI, CHF, aortic dissection, acute pulmonary edema, ARF, and
hypertensive encephalopathy

BP Management in Acute Ischemic Stroke
The use of IV Nicardepine is reasonable, readily available, easy to administer
and titrate, has short duration of action, and does not significantly affect ICP.
Although rare in acute ischemic stroke, arterial hypotension (a baseline
SBP<100mmHg, or DBP<70mmHg) higher rates of neurological
worsening, poor neurological outcomes, or death.
The cause of arterial hypotension should be determined and addressed (e.g.,
aortic dissection, volume depletion, blood loss, and decreased CO sec to MI
or cardiac arrhythmias)
BP Management in Acute Ischemic Stroke
In acute ischemic stroke, autoregulation is paralyzed in the affected tissues with CBF
passively following MAP. Rapid BP lowering further decrease in perfusion at the
penumbra.
Hypertension is typically present in acute stroke, with spontaneous decline in the first 5-
7days with attainment of neurological stability. SBP dropped by 28% during the
first day whether or not medications were given.
SBP and DBP drops of >20mmHg were associated with early neurological
worsening, high rates of poor outcome or death, and larger volumes of infarctions.

Rationale for Permissive Hypertension:
Treat if SBP > 180 mmHg
Acute lowering of SBP to 140mmHg within 7 days is safe and improves
outcome in patients with small-moderate size ICH not requiring surgical
intervention
If ICP monitor is available, keep CPP >70mmHg
BP Management in Acute Hypertensive ICH
Treat hypertension with modest reductions in BP to minimize vasospasm
and delayed cerebral ischemia
Preoperatively, for unsecured aneurysms, the use of IV Nicardepine to a
target SBP <150mmHg is reasonable.
BP Management in Acute SAH
1. Avoid HYPOTENSION and allow permissive hypertension during the first (7) days.
2. Avoid HYPOXEMIA
Routine O
2
is not warranted for all stroke patients unless theres evidence of hypoxemia
or desaturation (target SO
2
>94%)
Monitor oxygenation via pulse oximeter and/or determine ABG
Provide ventilator support if the upper airway is threatened, sensorium is impaired, or
ICP is increased.

2. Avoid HYPOXEMIA
3. Avoid HYPERGLYCEMIA or HYPOGLYCEMIA
Hyperglycemia causes lactic acidosis, increases free radical production, worsens cerebral edema, and
weakens blood vessels
Hypoglycemia can mimic a stroke
Achieve glucose targets of 140-180mg/dl if the FBS is >140mg/dl or RBS is
consistently >180mg/dl
2. Avoid HYPOXEMIA
Use an established and standardized IV insulin protocol for pxs who present with
extreme or persistent hyperglycemia, are critically ill, or who have received thrombolytic
therapy for at least the first 24-48hrs of hospitalization SQ basal long-acting insulin
+ rapid-acting insulin
For pxs who are feeding, add rapid-acting prandial (meal) insulin
Avoid D5 IV fluids
2. Avoid HYPOXEMIA
4. Avoid HYPERTHERMIA
Associated with poor outcome metabolic demand, free radical production, enhanced
neurotransmitter release
RR of 1-year mortality by 3.4 times
Treat fever with antipyretics and cooling blankets. Investigate for source of fever (e.g.,
infection)
Neuroprotective and Neurorestorative Drugs
Cerebrolysin
Citicoline
NeuroAID

The use of drugs with neurorestorative and
neuroprotective properties in acute stroke remains as a
matter of preference of the attending physician.
ANTICOAGULATION IN
ACUTE CARDIOEMBOLIC STROKE
Sources of Cardioembolic Stroke

Low or Uncertain Risk High Risk
MVP
Mitral annular calcification
Patent Foramen Ovale (PFO)
Atrial Septal Aneurysm
Calcific aortic stenosis
Mitral valve strands
AF (valvular or non-valvular)
Rheumatic MS
Prosthetic heart valves
Recent MI
LV/LA thrombus
Atrial myxoma
IE
Dilated cardiomyopathy
Marantic endocarditis
ANTICOAGULATION IN
Features Suggestive of Cardioembolic Stroke
Sudden onset of maximal deficit (<5 min)
Decreased level of consciousness
Rapid regression of initially massive symptoms (spectacular shrinking deficit)
Wernickes aphasia or global aphasia without hemiparesis
Visual field abnormalities

ANTICOAGULATION IN
Features Suggestive of Cardioembolic Stroke
Onset of symptoms after a Valsalva-provoking activity (e.g., coughing, bending)
Infratentorial ischemic stroke (cerebellar, PCA, and multi-level infarcts, top-of-the basilar
syndrome)
Hemorrhagic transformation and early recanalization of occluded intracranial vessel
Neuroimaging finding of acute infarcts involving multiple vascular territories in the brain
(predominantly carotid and MCA territories), or multiple levels of the posterior circulation

ANTICOAGULATION IN
Indications and Contraindications for Anticoagulation in Patients with
Cardioembolic Stroke

Probably Indicated Contraindicated
Intracardiac thrombus
Mechanical prosthetic valve
Recent MI
CHF
Bridging measure for long-term
coagulation

Bleeding diathesis
Non-petechial intracranial
hemorrhage
Recent major surgery or trauma
Infective endocarditis
ANTICOAGULATION IN
How to anticoagulate
Heparin 600-800 units per hour TIV via infusion pump. Heparin bolus IS NOT recommended.
Perform aPTT as often as necessary, every 4-6hrs after dose adjustments, to keep aPTT
levels at 1.5-2.5x the control
Infusion may be discontinued once oral anticoagulation with warfarin has reached
therapeutic levels or once antiplatelet medication is initiated for secondary prevention.

ANTICOAGULATION IN
The benefits of reducing early stroke recurrence should be weighed against the risk of
hemorrhagic transformation
higher in patients with large infarction, severe strokes or neurologic deficits, and
uncontrolled hypertension

MANAGEMENT OF
INCREASED INTRACRANIAL
PRESSURE
MANAGEMENT OF INCREASED ICP
Signs and Symptoms of Increased ICP
Deteriorating level of sensorium
Cushings triad: hypertension, bradycardia, irregular respiration
Anisocoria
General
Control agitation and pain with short-acting medications, such as NSAIDs and opioids.
Treat fever aggressively. Avoid hyperthermia.
Control seizures if present.
Phenytoin 18-20mg/kg LD slow IV, then maintained at 3-5 mg/kg; or
Levetiracetam 500mg IV q12
Strict blood glucose control between 140-180mg/dl
General
Maintain normal fluid and electrolyte balance
Avoid excessive free water or any hypotonic fluids such as D5W
Maintain normal volume status
Encourage hyperosmolar state with hypertonic saline and/or induce free water clearance
with mannitol or diuretics
Use stool softeners to prevent straining
Specific
Elevate the head at 30-45 degrees to assist venous drainage.
Do CSF drainage in the setting of hydrocephalus.
Administer osmotic therapy:
Give Mannitol 20% IV infusion: 0.5-1.5g/kg q 3-6h
Hypertonic saline is an option
Always maintain serum osmolality at 300-320mosmol/kg
Specific
Hyperventilate only in impending herniation by adjusting tidal volume (target pCO
2

levels of 30-35mmHg)
Carefully intubate patients with respiratory failure defined as:
SO
2
< 90% by pulse oximeter
By ABG: PaO
2
< 60 mmHg, and/ or PaCO
2
> 55mmHg
Consider surgical evacuation or decompressive hemicraniectomy if indicated
ICP catheter insertion
GUIDELINES FOR
ANTIPLATELET THERAPY IN
NONCARDIOEMBOLIC
STROKE OR TRANSIENT
ISCHEMIC ATTACK
GUIDELINES FOR ANTIPLATELET THERAPY IN
NONCARDIOEMBOLIC STROKE OR TRANSIENT ISCHEMIC
ATTACK
Patients without contraindication should receive antiplatelet agents to reduce
the risk of recurrent stroke and other cardiovascular events.
Long term ASA (80-100 mg/day) monotherapy, or the combination of ASA
25mg & ER Dipyridamole 200mg BID, Clopidogrel 75mg OD, Cilostazol
100mg BID, or Triflusal 300mg BID are all acceptable options for initial
therapy.
The selection of an antiplatelet agent should be individualized. Consider
cost, patient risk factor profiles, tolerance, and other clinical characteristics.

ATTACK
The combination of ASA and clopidogrel might be considered for initiation
within 24 hrs and continued within 90days of a minor ischemic stroke or
TIA.
The combination of ASA and clopidogrel when continued for 2-3yrs
increases the risk of hemorrhage and is not recommended for routine long
term secondary prevention after ischemic stroke or TIA.
For patients who have an ischemic stroke or TIA while taking ASA, there is
no evidence that increasing the dose of ASA provides additional benefit.

ATTACK
Although often considered for patients who have an ischemic stroke or TIA
while already on ASA, there is insufficient evidence to show that switching to
an alternative antiplatelet agents or the use of antiplatelet combination
reduces the risk for subsequent events.
It is recommended that patients who develop recurrent stroke while on
antithrombotic therapy be re-evaluated for pathophysiology and risk factors.

A good history and physical examination of patients could not be
overemphasized.
Identification of stroke mimickers should be facilitated to rule out other
possible diagnoses.
Comorbid conditions should be addressed adequately.
In our setting, there should be a conscious effort in the judicious use of
diagnostic examinations to maximize our resources in the management of
stroke patients.
Care of critically ill patients is a TEAM EFFORT.
Guidelines are guidelines. Management of patients should be individualized
depending on the patients clinical profile.
Talk to your patients and their relatives.
We are not GOD but we can be ANGELS.
DIOS MABALOS

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