Stroke guidelines, 2015

Cerebrovascular Accident
(Stroke)
Let’s guideline our minds!!
Usama Ragab Yousif (Msc.)
Internal Medicine Department

Agenda
• To be able to differentiate
between stroke and other
conditions
• To discuss the latest stroke
treatment strategies (either
interventional or non
interventional)
• To emphasize the role of early evaluation and
management of stroke patients

Disease makes men more physical, it leaves
them nothing but body.
Thomas Mann

Epidemiology
• Globally, about 17
million strokes occur
every year and stroke is
the second leading
cause of death after
coronary heart disease,
and the third most
common cause of
disability.
1- Krishnamurthi RV: Lancet Glob Health. 2013;1(5):e259.
Figure: http://www.who.int/mediacentre/factsheets/fs310/en/

Epidemiology
• Globally, the incidence of stroke due to ischemia is 68
%, while the incidence of hemorrhagic stroke
(intracerebral hemorrhage and subarachnoid
hemorrhage combined) is 32 %.
• Men have a higher incidence of stroke than women at
younger but not older ages, with the incidence reversed
and higher for women by age 75 years and older.
Mikulik R: J Intern Med 2015; 278: 145–165.
Lozano R, et al: Lancet. 2012 Dec;380(9859):2095-128.

Pathophysiology of Ischemic stroke
Normal cerebral blood flow (CBF): > 50
mL/100gm/min of brain tissues.1
18-50 mL/100gm/min of brain = oligemia.
Less than 18 mL/100gm/min of brain =
neurological deficit due to electrical failure
(transiant; TIA or permanent; infarction)
 < 8 mL = core infarction.
8-18 mL/100gm/min of brain = Penumbra
1- Cipolla MJ. The Cerebral Circulation. San Rafael (CA):
Morgan & Claypool Life Sciences; 2009.
Figure: P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248.
Print.

Penumbra is zone of reversible
ischemia around core of irreversible
infarction—salvageable in first few
hours after
ischemic stroke onset
Penumbra damaged by:
• Hypoperfusion
• Hyperglycemia
• Fever
• Seizure
http://www.strokecenter.org/professionals/brain-
anatomy/cellular-injury-during-ischemia/the-ischemic-
penumbra/ (HON code certified)

Sir Winston Churchill
Prime Minister of the United Kingdom from
1940 to 1945 and again from 1951 to 1955
Famous People Who Died of Stroke
http://www.ranker.com/list/famous-people-who-died-of-stroke/reference

Risk factors for stroke
POTENTIALLY Modifiable risk factorsFixed risk factors
Blood pressure
Cigarette smoking
Hyperlipidaemia
Heart disease
Atrial fibrillation
Congestive cardiac failure
Infective endocarditis
Diabetes mellitus
Excessive alcohol intake
Oestrogen-containing drugs
Polycythaemia
Age
Gender (male > female except at
extremes of age)
Race (Afro-Caribbean > Asian >
European)
Previous vascular event
 Myocardial infarction
 Stroke
Peripheral vascular disease
Heredity
High fibrinogen
P, Langhorne. "Stroke Disease." Davidson’s Principles and Practice of Medicine. 22nd ed. N.p.: Elsevier, 2014. 1231-248. Print.

Risk factors for stroke (cont.)
TIA is a risk factor for future stroke
SC Johnston et al: Validation and refinement of score to predict very early stroke risk after transient ischaemic attack.
Lancet 369:283, 2007.

CommentABCD2
Hospital observation may
be unnecessary
0-3
Hospital observation
justified
4-5
Hospital observation
worthwhile
6-7

National Stroke Foundation, 2010
The NSF in 2010 discuss this point in their guideline:
Those identified as high risk (e.g. ABCD2 score >3 and/or those with any one of
the following AF, carotid territory symptoms or crescendo TIA, should be admitted
to a stroke unit (or where available referred to a specialist TIA clinic if the person
can be assessed within 24 hours) to facilitate rapid specialist assessment and
management (A).
Urgent brain imaging (preferably MRI with DWI), ‘urgent’ being immediately
where available, but within 24 hours). Carotid imaging should also be undertaken
urgently in patients with anterior circulation symptoms who are candidates for
carotid re-vascularisation (B).
Those identified as low risk (e.g. aBCD2 score <4 and without AF or carotid
territory symptoms or crescendo TIA should commence initial therapy (e.g. aspirin)
and then be managed in the community by a general practitioner or private
specialist or, where possible, be referred to a specialist TIA clinic and seen within
seven days (GPP).
National Stroke Foundation – Australia (2010)

Joseph Stalin
The leader of the Soviet Union from the
mid-1920s until his death in 1953

Review of Anatomy
• Blood reaches the brain through 2 systems:
1. The carotid system (Anterior Circulation)
2. The vertebral system (Posterior Circulation)

Presentation
• Sudden onset
• Focal neurological deficit
• Progresses over minutes to hours
• Depends on location
• Symptoms include:
 SUDDEN numbness or weakness of face, arm or leg
 SUDDEN confusion, trouble speaking or understanding.
 SUDDEN trouble with vison.
 SUDDEN trouble walking, dizziness, loss of balance or coordination.
 SUDDEN severe headache.

Presentation (cont.)

Time is BRAIN
• The longer the time period that the person remains
unresponsive, the less likely it is that the person will
recover.
• It has calculated that in a typical large-vessel acute
ischaemic stroke, about 1.9 million neurons die every
minute during which stroke is untreated, 14 billion
synapses, and 12 km (7.5 miles) of myelinated fibers are
destroyed.1
• The first few days after onset is critical.
1- Saver, J. L. (2006). Time is brain—quantified. Stroke, 37(1), 263-266.

Definition of Classes and Levels of Evidence
Used in AHA/ASA Recommendations
Conditions for which there is evidence for and/or general
agreement that the procedure or treatment is useful and
effective.
Class I
Conditions for which there is conflicting evidence and/or a
divergence of opinion about the usefulness/efficacy of a
procedure or treatment.
The weight of evidence or opinion is in favor of the procedure
or treatment.
Usefulness/efficacy is less well established by evidence or
opinion.
Class II
Class IIa
Class IIb
Conditions for which there is evidence and/or general
agreement that the procedure or treatment is not
useful/effective and in some cases may be harmful.
Class III
Stroke. 2013;44:870-947.

Definition of Classes and Levels of Evidence
Used in AHA/ASA Recommendations
Therapeutic recommendations
Data derived from multiple randomized clinical trials or
meta-analyses
Level of Evidence A
Data derived from a single randomized trial or
nonrandomized studies
Level of Evidence B
Consensus opinion of experts, case studies, or standard
of care
Level of Evidence C
Diagnostic recommendations
Data derived from multiple prospective cohort studies
using a reference standard applied by a masked evaluator
Level of Evidence A
Data derived from a single grade A study or 1 or more
case control studies, or studies using a reference
standard applied by an unmasked evaluator
Level of Evidence B
Consensus opinion of expertsLevel of Evidence C
Stroke. 2013;44:870-947.

Prehospital Evaluation and Management of
Potential Stroke Patients
Prehospital care providers should use prehospital stroke assessment tools, such as
the Los Angeles Prehospital Stroke Screen or Cincinnati Prehospital Stroke Scale
(Class I; Level of Evidence B).
Cincinnati Stroke
Scale (Smile,
Wave, Talk)
Interpretation: if any
of these 3 signs is
abnormal, the
probability of a
stroke is 72%

Assessment
You can use the easily memorized FAST assessment

• Patients should be transported rapidly to the closest available
certified primary stroke centers (PSC) or comprehensive stroke
centers (CSC) or, if no such centers exist, the most appropriate
institution that provides emergency stroke care as described in the
statement (Class I; Level of Evidence A).
• For patients with suspected stroke, EMS should bypass hospitals
that do not have resources to treat stroke and go to the closest
facility most capable of treating acute stroke (Class I; Level of
Evidence B).
• Delaying intravenous rtPA therapy until after transport in otherwise
eligible patients decreases the chance for a good outcome.

Not RecommendedRecommended
Do not initiate interventions for
hypertension unless directed by
medical commands
Assess and manage ABCs
Initiate cardiac monitoring
Provide supplemental oxygen to maintain O2
saturation >94%
Do not administer excessive IV
fluids
Establish IV access per local protocol
Do not administer dextrose-
containing fluids in nonhypoglycemic
patients
Determine blood glucose and treat accordingly
Do not administer medications by
mouth (maintain NPO)
Determine time of symptom onset or last known
normal, and obtain family contact information,
preferably a cell phone
Triage and rapidly transport patient to nearest most
appropriate stroke hospital
Do not delay transport for
prehospital interventions
Notify hospital of pending stroke patient arrival
During transfer:

Emergency Triage and Initial
Evaluation
Bock BF. Proceedings of a National Symposium on Rapid Identification and Treatment of Acute Stroke: Response System for Patients
Presenting With Acute Stroke. http://www.ninds.nih.gov/
TimeAction
≤10 minutesDoor to physician
≤15 minutesDoor to stroke team
≤25 minutesDoor to CT initiation
≤45 minutesDoor to CT interpretation
≤60 minutesDoor to drug (≥80% compliance)
≤3 hoursDoor to stroke unit admission
An organized protocol for the emergency evaluation of patients with suspected
stroke is recommended (Class I; Level of Evidence B). The goal is to complete an
evaluation and to begin fibrinolytic treatment within 60 minutes of the patient’s
arrival in an ED. Designation of an acute stroke team that includes physicians,
nurses, and laboratory/radiology personnel is encouraged.
!!!!!!!

Assessment (cont.)
The use of a stroke rating scale, preferably the NIH Stroke Scale (NIHSS), is
recommended (Class I; Level of Evidence B).

ScoreStroke Severity
0No Stroke Symptoms
1-4Minor Stroke
5-15Moderate Stroke
16-20Moderate to Severe Stroke
21-42Severe Stroke
NIH Stroke Scale (cont.)
 The NIHSS has been found to be an excellent predictor of patient outcomes.
 A baseline NIHSS score greater than 16 indicates a strong probability of patient
death, while a baseline NIHSS score less than 6 indicates a strong probability of a
good recovery.
 On average, an increase of 1 point in a patient’s NIHSS score decreases the
likelihood of an excellent outcome by 17%.
 However, correlation between functional recovery and NIHSS scores was weaker
when the stroke was isolated to the cortex.
Neurology 53 (1): 126–131.

Assessment (cont.)
Teasdale G, Jennett B. (1974). "Assessment of coma
and impaired consciousness. A practical
scale.". Lancet 13 (2): 81–4.
Glasgow Coma Scale:
The Glasgow Coma Scale or GCS is
a neurological scale that aims to give a
reliable, objective way of recording the
conscious state of a person for initial as well as
subsequent assessment. A patient is assessed
against the criteria of the scale, and the
resulting points give a patient score between 3
(indicating deep unconsciousness) and either
14 (original scale) or 15 (the more widely used
modified or revised scale).

A limited number of hematologic, coagulation, and biochemistry tests are
recommended during the initial emergency evaluation, and only the assessment of
blood glucose must precede the initiation of intravenous rtPA (Class I; Level of
Evidence B).
I should be aware of stroke mimics!!!!!
Assessment (cont.)
‘Functional’ stroke mimics‘Structural’ stroke mimics
Todd’s paresis (after epileptic seizure)
Hypoglycaemia
Migrainous aura (with or without
headache)
Focal seizures
Ménière’s disease or other vestibular
disorder
Conversion disorder
Encephalitis
CO2 narcosis
Primary cerebral tumours
Metastatic cerebral tumours
Subdural haematoma
Cerebral abscess
Peripheral nerve lesions (vascular or
compressive)
Demyelination

Immediate Diagnostic Studies: Evaluation of a
Patient With Suspected Acute Ischemic Stroke
Stroke. 2013;44:870-947.
*Fibrinolytic therapy should not be delayed while awaiting the results unless:
(1) there is clinical suspicion of a bleeding abnormality or thrombocytopenia.
(2) the patient has received heparin or warfarin.
(3) the patient has received other anticoagulants (direct thrombin inhibitors or direct
factor Xa inhibitors).

Immediate Diagnostic Studies: Evaluation of a
Patient With Suspected Acute Ischemic Stroke
Stroke. 2013;44:870-947.

 Baseline electrocardiogram assessment is recommended in patients
presenting with acute ischemic stroke but should not delay initiation of
intravenous rtPA (Class I; Level of Evidence B).
 Baseline troponin assessment is recommended in patients presenting with
acute ischemic stroke but should not delay initiation of intravenous rtPA
(Class I; Level of Evidence C).
 The usefulness of chest radiographs in the hyperacute stroke setting in the
absence of evidence of acute pulmonary, cardiac, or pulmonary vascular
disease is unclear. If obtained, they should not unnecessarily delay
administration of fibrinolysis (Class IIb; Level of Evidence B).
Assessment (cont.)

Assessment (cont.)
Recommendations for Patients With Acute Cerebral Ischemic Symptoms
That Have Not Yet Resolved
 Emergency imaging of the brain is recommended before initiating any specific
therapy to treat acute ischemic stroke (Class I; Level of Evidence A). In most
instances, NECT will provide the necessary information to make decisions
about emergency management.
 Either NECT or MRI is recommended before intravenous rtPA administration to
exclude ICH (absolute contraindication) and to determine whether CT
hypodensity or MRI hyperintensity of ischemia is present (Class I; Level of
Evidence A).
 Intravenous fibrinolytic therapy is recommended in the setting of early ischemic
changes (other than frank hypodensity) on CT(Class I; Level of Evidence A).
Frank hypodensity on NECT may increase the risk of hemorrhage with
fibrinolysis. If frank hypodensity involves more than one third of the MCA
territory, intravenous rtPA treatment should be withheld (Class III; Level of
Evidence A).

Assessment (cont.)
That Have Not Yet Resolved (cont.)
NECT should be obtained within 25 minutes of the patient’s arrival in the ED.
NECT definitively excludes parenchymal hemorrhage and can assess other
exclusion criteria for intravenous rtPA, such as widespread hypoattenuation.
CommentsIts use in acute ischemic stroke
However, the ability of observers to
detect these early infarct signs on
NECT is quite variable and occurs in
≤67% of cases imaged within 3 hours.
A sign of cerebral ischemia within the
first few hours after symptom onset on
NECT is loss of gray-white
differentiation.
This sign has approx. 100% sensitivity,
however only 30% specificity.
Increased density within the occluded
artery, such as the hyperdense middle
cerebral artery (MCA) sign, indicative
of large-vessel occlusion.
The sensitivity is low (38%) but the
specificity is 100%.
Hyperdense MCA “dot” sign.

Assessment (cont.)
Infarction appears as hypodense (more dark) area on CT

Assessment (cont.)
Which become denser with time
Case courtesy of Dr David Cuete, Radiopaedia.org, rID: 35732

Assessment (cont.)
Loss of grey-white differentiation
Case courtesy of Dr David Cuete, Radiopaedia.org, rID: 35427

Assessment (cont.)
Hyperdense MCA sign
Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 5105
Case courtesy of Dr Jeremy Jones, Radiopaedia.org, rID: 13190
Case courtesy of Dr Mohammed Alghamdi, Radiopaedia.org, rID: 17138

Assessment (cont.)
MCA dot sign
Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 25414

Assessment (cont.)
So,……
Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 25414

What about MRI….
For diagnosing ischemic stroke in the emergency setting:
CT scans (without contrast enhancements):
sensitivity= 16%specificity= 96%
MRI scan:
MRI reliably documents the extent and location of infarction in all areas of the
brain, including the posterior fossa and cortical surface.
MRI scanners with magnets of higher field strength produce more reliable and
precise images.
Diffusion-weighted imaging is more sensitive for early brain infarction than
standard MR sequences or CT, as is fluid-ttenuated
inversion recovery (FLAIR) imaging.

What about MRI….
Case courtesy of Dr G Balachandran, Radiopaedia.org, rID: 10704
Subtle hypointensity seen in right MCA
territory on T1, with increased signal on
T2 and FLAIR. DWI b=1000 shows the
brightest signal in right MCA territory
confirming the cytotoxic odema due to
hyperacute infarct.

Assessment (cont.)
 CT perfusion and MRI perfusion and diffusion imaging, including measures of
infarct core and penumbra, may be considered for the selection of patients for
acute reperfusion therapy beyond the time windows for intravenous fibrinolysis.
These techniques provide additional information that may improve diagnosis,
mechanism, and severity of ischemic stroke and allow more informed clinical
decision making (Class IIb; Level of Evidence B).

Assessment (cont.)
Using IV administration of gadolinium contrast, MR perfusion studies can be
performed. Brain regions showing poor perfusion but no abnormality on diffusion
provide, compared to CT, an equivalent measure of the ischemic penumbra.
ƒDWI is thought to show the area currently infarcting.ƒBut is there an “area at
risk” where blood flow is reduced but cells haven’t died yet?
ƒImaging this region (the penumbra) = goal of MR perfusion imaging.

Assessment(cont.)
A. Computed tomography (CT)
perfusion mean-transit time
map showing delayed
perfusion of the left MCA
distribution (blue).
B. Predicted region of infarct
(red) and penumbra (green)
based on CT perfusion data.
C. Conventional angiogram
showing occlusion of the left
internal carotid–MCA
bifurcation (b4 & after
successful thrombectomy).
D. The clot rmoved by
thrombectomy device.
E. CT scan of the brain 2 days
later; note infarction in the
region predicted in B but
preservation of the
penumbral region by
successful revascularization.

Assessment(cont.)
A. MRI diffusion-weighted image
(DWI) of an 82-year-old woman 2.5 h
after onset of right-sided weakness and
aphasia reveals restricted diffusion
within the left basal ganglia and internal
capsule (colored regions).
B. Perfusion defect within the left hemisphere
(colored signal) imaged (gadolinium contrast). The discrepancy between
the region of poor perfusion shown in B and the diffusion deficit shown in
A is called diffusion-perfusion mismatch and provides an estimate of the
ischemic penumbra.
C. Fluid-attenuated inversion recovery image obtained 3 days later
showing a region of infarction (coded as white) that corresponds to the
initial DWI image in A, but not the entire area at risk shown in B,
suggesting that successful embolectomy

Assessment (cont.)
Recommendations for Patients With Cerebral Ischemic Symptoms That
Have Resolved
 Noninvasive imaging of the cervical vessels should be performed routinely
as part of the evaluation of patients with suspected TIAs (Class I; Level of
Evidence A).
 Noninvasive imaging by means of CTA or MRA of the intracranial
vasculature is recommended to exclude the presence of proximal
intracranial stenosis and/or occlusion (Class I; Level of Evidence A).
 Patients with transient ischemic neurological symptoms should undergo
neuroimaging evaluation within 24 hours of symptom onset or as soon as
possible in patients with delayed presentations. MRI, including DWI, is the
preferred brain diagnostic imaging modality. If MRI is not available, head CT
should be performed (Class I; Level of Evidence B).

Assessment (cont.)
Cerebral Angiography
 Conventional x-ray cerebral angiography is the gold standard for identifying
and quantifying atherosclerotic stenoses of the cerebral arteries and for
identifying and characterizing other pathologies, including aneurysms,
vasospasm, intraluminal thrombi, fibromuscular dysplasia, arteriovenous
fistulae, vasculitis, and collateral channels of blood flow.
 Conventional angiography carries risks of arterial damage, groin hemorrhage,
embolic stroke, and renal failure from contrast nephropathy, so it should be
reserved for situations where less invasive means are inadequate.

Assessment (cont.)
Carotid Doppler US:
Stenosis more than 70% should raise our mind to possible intervention

Repeating Neuroimaging
A repeat brain Ct or MRI and acute medical review should be considered
urgently when a patient’s condition deteriorates. (GPP)

General Supportive Care and Treatment of
Acute Complications
The era of interventional therapy
NINDS* and ASA** Recommended Stroke Evaluation Time Benchmarks for
Potential Thrombolysis Candidate
*National Institute of Neurological Disorders and Stroke
**American Stroke Association
Time Interval Time Target
Door to doctor 10 min
Access to neurologic
expertise
15 min
Door to CT scan completion 25 min
Door to CT scan interpretation 45 min
Door to treatment 60 min
Admission to stroke unit or
ICU
3 h

Treatment (cont.)
Factors Recommendation
Airway
&Breathing
Airway support and ventilatory assistance are recommended for the
treatment of patients with acute stroke who have decreased consciousness or
who have bulbar dysfunction that causes compromise of the airway (Class I;
Level of Evidence C).
Supplemental oxygen should be provided to maintain oxygen saturation
>94% (Class I; Level of Evidence C).
Supplemental oxygen is not recommended in nonhypoxic patients with
acute ischemic stroke (Class III; Level of Evidence B).
Blood
Glucose
Hypoglycemia (blood glucose <60 mg/dL) should be treated in patients with
acute ischemic stroke (Class I; Level of Evidence C). The goal is to achieve
levels of 140-180 mg/dL (Class IIa; Level of Evidence C).
Nutrition A formal screening procedure for dysphagia should be performed in all
patients before the initiation of oral intake to reduce the risk of pneumonia
Insert a nasogastric tube if the patient fails the swallow test.
Consider PEG only if prolonged enteral feeding is required (Class I; Level
of Evidence B).
Stroke. 2013;44:870-947.

Infection and
fever
Sources of hyperthermia (temperature >38°C) should be identified and
treated, and antipyretic medications should be administered to lower
temperature (Class I; Level of Evidence C).
Routine use of prophylactic antibiotics has not been shown to be
beneficial (Class III; Level of Evidence B).
Patients with suspected pneumonia or urinary tract infections should be
treated with appropriate antibiotics (Class I; Level of Evidence A).
Hypovolemia Hypovolemia should be corrected with intravenous normal saline, and
cardiac arrhythmias that might be reducing cardiac output should be
corrected (Class I; Level of Evidence C).
Seizures Clinical seizures should be treated with antiseizure drugs (Class I;
Level of Evidence B).
Prophylactic antiseizure medication is not recommended (Class III;
Prolonged
recumbency
Subcutaneous administration of anticoagulants is recommended for
treatment of immobilized patients with ischemic infarction to prevent deep
vein thrombosis (Class I; Level of Evidence A).
The use of aspirin is reasonable for treatment of patients who cannot
receive anticoagulants for prophylaxis of deep vein thrombosis (Class IIa;
Level of Evidence A).
Treatment (cont.)

Hypertension in acute stroke a
management dilemma
Ischemic stroke
The treatment of arterial hypertension immediately after stroke is problematic.
Observational studies have found that a rapid and steep reduction in BP during
the first 24 h after stroke onset might be harmful.1-2
Two important pathophysiologic processes should be considered during
management of acute stroke. These are:
1. Impaired cerebral autoregulation.
2. Increased intracranial pressure (ICP).
In patients with ischemic stroke, perfusion pressure distal to the obstructed vessel
is low, and the distal vessels are dilated. Thus, elevated BP is necessary to maintain
brain perfusion in borderline ischemic areas3
. Lowering of BP in patients with acute
ischemic stroke has been associated with clinical deterioration.
1- Stroke 2004; 35:520–527. 2- Neurology 2003; 61:1047–1051. 3- Stroke 2009; 40:2251–2256.

management dilemma (cont.)
Kaplan, NM. Management of hypertensive emergencies. Lancet 1994; 344:1335.

The guidelines:
In patients with markedly elevated blood pressure who do not receive fibrinolysis,
a reasonable goal is to lower blood pressure by 15% during the first 24 hours after
onset of stroke. The level of blood pressure that would mandate such treatment is
not known, but consensus exists that medications should be withheld unless the
systolic blood pressure is >220 mm Hg or the diastolic blood pressure is >120
mmHg. (Class I; Level of Evidence C)
If BP is not maintained at or below 185/110 mmHg, do not consider administering
recombinant tissue plasminogen activator (rtPA). During and after thrombolytic
therapy, BP should be maintained below 180/105 mmHg for at least 24 h (Class I;
Level of Evidence B)
Circulation 2010; 122 (Suppl 3): S818–S828.
Stroke. 2013;44:870-947.

The guidelines:
Evidence from one clinical trial indicates that initiation of antihypertensive therapy
within 24 hours of stroke is relatively safe. Restarting antihypertensive medications
is reasonable after the first 24 hours for patients who have preexisting hypertension
and are neurologically stable unless a specific contraindication to restarting
treatment is known (Class IIa; Level of Evidence B).
No data are available to guide selection of medications for the lowering of blood
pressure in the setting of acute ischemic stroke. (Class IIa; Level of Evidence C).
Stroke. 2013;44:870-947.

The guidelines:
Many patients have spontaneous declines in blood pressure during the first 24
hours after onset of stroke. Until more definitive data are available, the benefit of
treating arterial hypertension in the setting of acute ischemic
stroke is not well established (Class IIb; Level of Evidence C). Patients who have
malignant hypertension or other medical indications for aggressive treatment of
blood pressure should be treated accordingly.
Pre-existing antihypertensive therapy can be continued (orally or via nasogastric
tube) provided there is no symptomatic hypotension or other reason to withhold
treatment is considered a good practice point (GPP) according to National Stroke
Foundation, 2010.
Stroke. 2013;44:870-947.

American Heart Association/American Stroke Association. Stroke. 2013;44:870–947.
Inclusion criteria:
Diagnosis of ischemic stroke causing measurable neurological deficit
Onset of symptoms <3 hours before beginning treatment
Aged ≥18 years
Exclusion criteria:
χSignificant head trauma or prior stroke in previous 3 months
χSymptoms suggest subarachnoid hemorrhage
χArterial puncture at noncompressible site in previous 7 days
χHistory of previous intracranial hemorrhage
χIntracranial neoplasm, arteriovenous malformation, or aneurysm
χRecent intracranial or intraspinal surgery
χElevated blood pressure (systolic >185 mm Hg or diastolic >110 mm Hg)
χActive internal bleeding
The American Heart Association/American Stroke Association (AHA/ASA)
inclusion guidelines for the administration of rt-PA in under 3 hours are as
follows:
Thrombolytic therapy

Exclusion criteria (cont.):
χAcute bleeding diathesis
χPlatelet count <100 000/mm³
χHeparin received within 48 hours, resulting in abnormally elevated aPTT
greater than the upper limit of normal
χCurrent use of anticoagulant with INR >1.7 or PT >15 seconds
χCurrent use of direct thrombin inhibitors or direct factor Xa inhibitors with
elevated sensitive laboratory tests (such as aPTT, INR, platelet count, and ECT;
TT; or appropriate factor Xa activity assays)
χBlood glucose concentration <50 mg/dL (2.7 mmol/L)
χCT demonstrates multilobar infarction (hypodensity >1/3 cerebral hemisphere)

Treatment Recommendations
rTPA In selected patients presenting within 3 hours: IV rt-Pa (0.9mg/kg,
maximum 90mg ) with 10% given as a bolus followed by an infusion over
one hour (Class I; Level of Evidence A).
Patients eligible for intravenous r-tPA should receive intravenous r-tPA
even if endovascular treatments are being considered (Class I; Level of
Evidence A).
In patients eligible for intravenous rtPA, benefit of therapy is time
dependent, and treatment should be initiated as quickly as possible. The
door-to-needle time (time of bolus administration) should be within 60
minutes from hospital arrival (Class I; Level of Evidence A).
Intravenous rtPA (0.9 mg/kg, maximum dose 90 mg) is recommended for
administration to eligible patients who can be treated in the time period of
3 to 4.5 hours after stroke onset (Class I; Level of Evidence B).
Treatment (cont.)

rTPA Intravenous rtPA is reasonable in patients whose blood pressure can be
lowered safely (to below 185/110 mm Hg) with antihypertensive agents,
with the physician assessing the stability of the blood pressure before
starting intravenous rtPA (Class I; Level of Evidence B).
In patients undergoing fibrinolytic therapy, physicians should be aware of
and prepared to emergently treat potential side effects, including bleeding
complications and angioedema that may cause partial airway obstruction
Intravenous rtPA is reasonable in patients with a seizure at the time of
onset of stroke if evidence suggests that residual impairments are
secondary to stroke and not a postictal phenomenon (Class IIa; Level of
Evidence C).
Treatment (cont.)

rTPA The usefulness of intravenous administration of tenecteplase, reteplase,
desmoteplase, urokinase, or other fibrinolytic agents and the intravenous
administration of ancrod or other defibrinogenating agents is not well
established, and they should only be used in the setting of a clinical trial
(Class IIb; Level of Evidence B).
The intravenous administration of streptokinase for treatment of stroke is
not recommended (Class III; Level of Evidence A).
The use of intravenous rtPA in patients taking direct thrombin inhibitors or
direct factor Xa inhibitors may be harmful and is not recommended unless
sensitive laboratory tests such as aPTT, INR, platelet count, and TT, or
appropriate direct factor Xa activity assays are normal, or the patient has
not received a dose of these agents for >2 days (assuming normal renal
metabolizing function). Similar consideration should be given to patients
being considered for intra-arterial rtPA (Class III; Level of Evidence C).
Treatment (cont.)

The effectiveness of intravenous treatment with rtPA is not well established (Class
IIb; Level of Evidence C) and requires further study for patients who can be
treated in the time period of 3 to 4.5 hours after stroke but have 1 or more of the
following exclusion criteria: (1) patients >80 years old, (2) those taking oral
anticoagulants, even with INR ≤1.7, (3) those with a baseline NIHSS score >25, or
(4) those with a history of both stroke and diabetes mellitus.

J Stroke Cerebrovasc Dis. 2014;23:2130–2138.
Survey of US stroke clinicians
on their willingness to treat
with recombinant tissue-type
plasminogen activator (rtPA)
in the setting of each
individual rtPA exclusion
criteria.

Neuroprotective
Agents
The utility of induced hypothermia for the treatment of patients with
ischemic stroke is not well established, and further trials are recommended
(Class IIb; Level of Evidence B).
At present, no pharmacological agents with putative neuroprotective
actions have demonstrated efficacy in improving outcomes after ischemic
stroke, and therefore, other neuroprotective agents are not recommended
(Class III; Level of Evidence A) = NSF, 2010 guidelines
Routine use of nutritional supplements has not been shown to be
Anticoagulant
s
Guidelines: Guidelines issued in 2013 by the American
Heart Association/American Stroke Association state that urgent
anticoagulation is not recommended for the treatment of patients with acute
ischemic stroke. Similarly, 2012 guidelines from the American College of
Chest Physicians (ACCP) recommend early aspirin therapy over
therapeutic parenteral anticoagulation for patients with acute ischemic
stroke or transient ischemic attack (TIA).
Treatment (cont.)
Stroke. 2013;44:870-947. Chest 2012; 141:e601S National Stroke Foundation – Australia (2010)

Anticoagulant
s
Guidelines: As well NSF, guideline in 2010 have discussed this point
and clearly stated that: the routine use of early anticoagulation in unselected
patients following ischaemic stroke/TIA is not recommended (A).
Treatment (cont.)

Anti Coagulation following Acute non
hemorrhagic Stroke
 While parenteral anticoagulation is not recommended during the first 48 hours
after acute ischemic stroke, oral anticoagulation is recommended for secondary
stroke prevention in patients with atrial fibrillation and other high-risk sources of
cardiogenic embolism (see later).
 The timing of its initiation for such patients is mainly dependent on the size of the
infarct, which is presumed to correlate with the risk of hemorrhagic
transformation. Thus, for medically stable patients with a small or moderate-
sized infarct, warfarin can be initiated soon (after 24 hours) after admission with
minimal risk of transformation to hemorrhagic stroke (however this still a matter
of debate), while withholding anticoagulation for two weeks is generally
recommended for those with 1large infarctions, 2symptomatic hemorrhagic
transformation, or 3poorly controlled hypertension.

Atrial fibrillation and cardioembolic
stroke
A subject of intense debate is the role of immediate anticoagulation with heparin in
stroke patients with atrial fibrillation (AF).
A 2007 meta-analysis examined seven trials involving 4624 patients and compared
heparin or low molecular weight heparins started within 48 hours for acute
cardioembolic stroke with other treatments (aspirin or placebo). The following
observations were reported:
●Anticoagulants were associated with a statistically non significant reduction in
recurrent ischemic stroke within 7 to 14 days (3.0 vs. 4.9 %, odds ratio [OR] 0.68,
95% CI 0.44-1.06)
●Anticoagulants were associated with a statistically significant increase in
symptomatic intracranial hemorrhage (2.5 vs. 0.7 %, OR 2.89, 95% CI 1.19-7.01)
●Anticoagulants and other treatments had a similar rate of death or disability at final
follow-up (≈ 74%)
Thus, the results do not support early anticoagulant
treatment of acute cardioembolic stroke
Paciaroni M, et al. Stroke 38.2 (2007): 423-430.

A systematic review updated in 2015 examined the effect of anticoagulant therapy
vs. control in the early treatment of patients with acute ischemic stroke. This review
included 24 trials involving 23,748 subjects.
The anticoagulants tested were standard unfractionated heparin, low molecular
weight heparins, heparinoids, oral anticoagulants, and thrombin inhibitors. The
following were the major findings:
●Based upon 11 trials (22,776 patients), anticoagulant therapy did not reduce the
odds of death from all causes (odds ratio 1.05, 95% CI 0.98-1.12).
●Based upon eight trials (22,125 patients), anticoagulants did not reduce the odds
of being dead or dependent at the end of follow-up (odds ratio 0.99, 95% CI 0.93-
1.04).
●Although full anticoagulant therapy was associated with about 9 fewer recurrent
ischemic strokes per 1000 patients treated, it was also associated with a 9 per 1000
increase in symptomatic intracranial hemorrhages.
Sandercock PA, Counsell C, Kane EJ. Anticoagulants for acute ischaemic stroke. Cochrane Database Syst Rev 2015; 3:CD000024.
Anti Coagulation following Acute non
hemorrhagic Stroke (con.)

Progressing stroke
(Stroke in evolution)
• Heparin was once widely used to treat patients who continued to
have neurologic deterioration in the first hours or days after ischemic
stroke.
• However the guidelines stated that: Urgent anticoagulation, with the
goal of preventing early recurrent stroke, halting neurological
worsening, or improving outcomes after acute ischemic stroke, is not
recommended for treatment of patients with acute ischemic stroke
(Class III; Level of Evidence A). Also recommended by
International stroke foundation, 2010 (A).
• Urgent anticoagulation for the management of noncerebrovascular
conditions is not recommended for patients with moderate-to-severe
strokes because of an increased risk of serious intracranial
hemorrhagic complications (Class III; Level of Evidence A).
Stroke. 2013;44:870-947. National Stroke Foundation – Australia (2010)

Anti Platelets following Acute Stroke
Recommendations
NICE, 2008
All people presenting with acute stroke who have had a diagnosis of primary intracerebral
haemorrhage excluded by brain imaging should, as soon as possible but certainly within 24
hours, be given (and continued for 2 weeks after onset of stroke):
aspirin 300 mg orally if they are not dysphagic or
aspirin 300 mg rectally or by enteral tube if they are dysphagic.
People with disabling ischaemic stroke who are in atrial fibrillation should be treated with
aspirin 300 mg for the first 2 weeks before considering anticoagulation treatment.
National Stroke Foundation Guidelines, 2010
 Aspirin orally or via a nasogastric tube or suppository (for those with dysphagia) should
be given as soon as possible after the onset of stroke symptoms (i.e. within 48 hours) if
Ct/MRI scans exclude haemorrhage. the first dose should be at least 150 to 300 mg.
Dosage thereafter can be reduced (e.g. 100 mg daily).(A)
National Institute for Health and Clinical Excellence (NICE) (2008): Stroke: Diagnosis and initial management of acute stroke and transient
ischaemic attack (TIA)

Recommendations
ACCP, 2012
 In patients with acute ischemic stroke or transient ischemic attack (TIA), we recommend
early (within 48 h) aspirin therapy at a dose of 160 to 325 mg over no aspirin therapy
(Grade 1A).
 In patients with acute ischemic stroke or TIA, we recommend early (within 48 h) aspirin
therapy with an initial dose of 160 to 325 mg over therapeutic parenteral anticoagulation
(Grade 1A).
 In patients with a history of ischemic stroke or TIA and atrial fibrillation, including
paroxysmal AF, who are unsuitable for or choose not to take an oral anticoagulant (for
reasons other than concerns about major bleeding), we recommend combination
therapy with aspirin and clopidogrel over aspirin (Grade 1B).
Chest . 2012;141(2_suppl):e601S-e636S.

Recommendations
ASA/AHA, 2013
 Oral administration of aspirin (initial dose
is 325 mg) within 24 to 48 hours after
stroke onset is recommended for
treatment of most patients (Class I; Level
of Evidence A).
 The usefulness of clopidogrel for the
treatment of acute ischemic stroke is not
well established (Class IIb; Level of
Evidence C).
 The use of aspirin is reasonable for
treatment of patients who cannot receive
anticoagulants for prophylaxis of deep
vein thrombosis (Class IIa; Level of
Evidence A).
The efficacy of intravenous tirofiban and
eptifibatide is not well established, and
these agents should be used only in the
setting of clinical trials (Class Iib; Level of
Evidence C).
Aspirin is not recommended as a
substitute for other acute interventions for
treatment of stroke, including intravenous
rtPA (Class III; Level of Evidence B).
The administration of other intravenous
antiplatelet agents that inhibit the
glycoprotein IIb/IIIa receptor is not
recommended (Class III; Level of
Evidence B).
Stroke. 2013;44:870-947.

The evidence….
Chinese Acute Stroke Trial (CAST)2International Stroke Trial (IST)1
21,100 patients19.435 patients with suspected acute
ischemic stroke
Patients allocated to aspirin (300 mg)
within 48 hours of symptom onset
60 mg of aspirin daily or placebo, also
within 48 hours of the onset of acute
ischemic stroke
Aspirin-allocated patients experienced
a 14 percent reduction in total
mortality at four weeks (3.3 versus 3.9
percent).
significant reductions in the 14-day
recurrence of ischemic stroke (2.8
versus 3.9 percent) and in the
combined outcome of nonfatal stroke
or death (11.3 versus 12.4 percent).
IST and CAST trials3
The combined data demonstrated a reduction in mortality of 13 per 1000
patients after several weeks to six months of follow-up
1- Lancet 1997; 349:1569. 2- Lancet 1997; 349:1641. 3- Stroke 2000; 31:1240.

What about Dual antiplatelet
agents
Circulation 2013; 128:1656.
 A 2013 meta-analysis of early dual antiplatelet therapy versus monotherapy for
patients with noncardioembolic acute ischemic stroke or TIA identified 14 trials
with over 9000 adults.
 Dual antiplatelet therapy significantly reduced risk of stroke recurrence (risk
ratio, 0.69; 95% confidence interval, 0.60-0.80; P<0.001) and the composite
outcome of stroke, TIA, acute coronary syndrome, and all death (risk ratio,
0.71; 95% confidence interval, 0.63-0.81; P<0.001) when compared with
monotherapy, and non significantly increased risk of major bleeding (risk ratio,
1.35; 95% confidence interval, 0.70-2.59, P=0.37).

agents
 In another study published in 2016, analysis of a prospective multicenter stroke
registry database from 14 hospitals in South Korea.
 Study subjects were divided into 3 groups according to the subsequent
antiplatelet therapy strategy pursued; maintaining aspirin monotherapy (MA
group), switching aspirin to nonaspirin antiplatelet agents (SA group), and
adding another antiplatelet agent to aspirin (AA group). The primary study end
point was the composite of stroke (ischemic and hemorrhagic), myocardial
infarction, and vascular death up to 1 year after stroke onset.
Stroke. 2016;47:128-134.

agents
Stroke. 2016;47:128-134.
Switching to or adding alternative antiplatelet agents could be associated with
reduction in future vascular events than maintaining aspirin monotherapy

Treatment of Acute Neurological
Complications
Patients with major infarctions are at high risk for complicating brain
edema and increased ICP. Measures to lessen the risk of edema and
close monitoring of the patient for signs of neurological worsening during
the first days after stroke are recommended (Class I; Level of Evidence
A).
Decompressive surgical evacuation of a space-occupying cerebellar
infarction is effective in preventing and treating herniation and brain stem
compression (Class I; Level of Evidence B).
Decompressive surgery for malignant edema of the cerebral
hemisphere is effective and potentially lifesaving (Class I; Level of
Evidence B).

Treatment (cont.)
Stroke. 2015;46:3020–3035.

Treatment (cont.)
Endovascular Treatment
Stroke. 2015;46:3020–3035.
1- Endovascular Treatment
Patients should receive endovascular therapy with a stent retriever if they meet
all the following criteria (Class I; Level of Evidence A):
a. Prestroke mRS score 0 to 1
b. Acute ischemic stroke receiving intravenous r-tPA within 4.5 hours of onset
according to guidelines from professional medical societies
c. Causative occlusion of the ICA or proximal MCA (M1),
d. Age ≥18 years,
e. NIHSS score of ≥6,
f. ASPECTS of ≥6, and
g. Treatment can be initiated (groin puncture) within 6 hours of symptom onset.

Score Description
0 No symptoms at all
1
No significant disability despite symptoms; able to carry out all usual
duties and activities
2
Slight disability; unable to carry out all previous activities, but able to
look after own affairs without assistance
3
Moderate disability; requiring some help, but able to walk without
assistance
4
Moderately severe disability; unable to walk without assistance and
unable to attend to own bodily needs without assistance
5
Severe disability; bedridden, incontinent, and requiring constant
nursing care and attention
6 Dead
Modified Rankin scale: a commonly used scale for measuring the degree of disability or dependence
in the daily activities of people who have suffered a stroke or other causes of neurological disability.
Van Swieten JC, Koudstaa PJ, Visser MC, et al. Interobserver agreement for the assessment of handicap in stroke patients.
Stroke 1988; 19:604.
Modified Rankin scale

Areas
caudate M1: "anterior MCA cortex," corresponding to frontal operculum
putamen M2: "MCA cortex lateral to insular ribbon" corresponding to anterior temporal lobe
internal capsule
M3: "posterior MCA cortex" corresponding to posterior temporal lobe
insular cortex
M4: "anterior MCA territory immediately superior to M1”
M5: "lateral MCA territory immediately superior to M2”
M6: "posterior MCA territory immediately superior to M3”
The Alberta stroke programe early CT score (ASPECTS)
Lancet. 2000;355 (9216): 1670-4.
Am J Neuroradiol. 2001;22 (8): 1534-42.
ASPECTS
It is a 10-point quantitative topographic CT scan score used in patients
with middle cerebral artery (MCA) stroke. Segmental assessment of the MCA
vascular territory is made and 1 point is deducted from the initial score of 10 for
every region involved:

Case courtesy of Dr Subash Thapa, Radiopaedia.org, rID: 40018
ASPECTS (cont.)

Treatment (cont.)
Stroke. 2015;46:3020–3035.
1- Endovascular Treatment (cont.)
As with intravenous r-tPA, reduced time from symptom onset to reperfusion
with endovascular therapies is highly associated with better clinical outcomes
When treatment is initiated beyond 6 hours from symptom onset, the
effectiveness of endovascular therapy is uncertain for patients with acute
ischemic stroke who have causative occlusion of the ICA or proximal MCA
(M1) (Class IIb; Level of Evidence C). Additional randomized trial data are
needed.
In carefully selected patients with anterior circulation occlusion who have
contraindications to intravenous r-tPA, endovascular therapy with stent
retrievers completed within 6 hours of stroke onset is reasonable (Class IIa;

Treatment (cont.)
Stroke. 2015;46:3020–3035.
1- Endovascular Treatment (cont.)
Although its benefits are uncertain, the use of endovascular therapy with
stent retrievers may be reasonable for patients with acute ischemic stroke in
whom treatment can be initiated (groin puncture) within 6 hours of symptom
onset and who have prestroke mRS score >1, ASPECTS <6, or NIHSS score
<6 and causative occlusion of the ICA or proximal MCA (M1) (Class IIb;
Level of Evidence B). Additional randomized trial data are needed.
Use of stent retrievers is indicated in preference to the MERCI device.
(Class I; Level of Evidence A).

Treatment (cont.)
The idea…..
The corkscrew
Embolectomy

Treatment (cont.)
Removal of the clot may be attempted in
those where it occurs within a large blood
vessel and may be an option for those who
either are not eligible for or do not improve
with intravenous thrombolytics.
The Merci Retrieval System

Treatment (cont.)
Allowing what is called giving
the brain a drink!!
Stent Retrievers: Solitaire® or Trevo ® systems

Treatment (cont.)
Remember; Time = Brain

Treatment (cont.)
Endovascular Treatment
Stroke. 2015;46:3020–3035.
2- Imaging prior endovascular treatment
The benefits of additional imaging beyond CT and CTA or MRI and MRA
such as CT perfusion or diffusion- and perfusion-weighted imaging for
selecting patients for endovascular therapy are unknown (Class IIb; Level of
Evidence C).

Emergency Diagnosis and Assessment
1. A baseline severity score should be performed as part of the initial
evaluation of patients with ICH (Class I; Level of Evidence B).
2. Rapid neuroimaging with CT or MRI is recommended to distinguish
ischemic stroke from ICH (Class I; Level of Evidence A).
3. CTA and contrast-enhanced CT may be considered to help identify patients
at risk for hematoma expansion (Class IIb; Level of Evidence B), and
CTA, CT venography, contrast-enhanced CT, contrastenhanced MRI,
magnetic resonance angiography and magnetic resonance venography, can
be useful to evaluate for underlying structural lesions including vascular
malformations and tumors when there is clinical or radiological suspicion
(Class IIa; Level of Evidence B).

• Maximum score described is 5 in which
% of mortality at 30 days is nearly 100%.
• Although an ICH Score of 6 is possible
with the scale, this is rarely observed and
is considered highly likely to be fatal.
ICH Score
JC Hemphill et al: Stroke 32:891, 2001; JC Hemphill et
al: Neurology 73:1088,2009.

Neuroimaging
 CT is very sensitive for identifying acute hemorrhage and is considered the
“gold standard”;
 Gradient echo and T2* susceptibility-weighted MRI are as sensitive as CT for
detection of acute hemorrhage and are more sensitive for identification of
prior hemorrhage.
 CT angiography (CTA) and contrast-enhanced CT may identify patients at
high risk of ICH expansion based on the presence of contrast within the
hematoma, often termed a spot sign. A larger number of contrast spots
suggests even higher risk of expansion.
 MRI, magnetic resonance angiography, magnetic resonance venography, and
CTA or CT venography can identify specific causes of hemorrhage, including
arteriovenous malformations, tumors, moyamoya, and cerebral vein
thrombosis.
Cerebrovasc Dis. 2013;35:582–589.

CT scans (without contrast enhancements):
MRI scan:
CT imaging is also sensitive for detecting SAH (although by itself does not rule it
out), and CTA can readily identify intracranial aneurysms.
On CT brain, hemorrhage appears as
hyperdense region, i.e. more white
Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 10598

The CT angiographic (CTA) spot sign is defined as unifocal or multifocal contrast
enhancement within an acute primary intracerebral haemorrhage (ICH) visible on
CTA source images and discontinuous from adjacent normal or abnormal blood
vessels . It should not be present on pre-contrast images. It corresponds to a site of
active, dynamic haemorrhage and is an independent predictor of ICH growth and
poor outcome
The CT angiographic (CTA) spot sign
Lancet Neurol. 2012;11 (4): 307-14.

Localization
CerebellarPontineBasal ganglia
10%10%80%

Investigations (cont.)
Modified Fisher scale on CT brain (predict risk of vasospasm):
Risk of vasospasmIVHSAH
24%-No or minimalGrade I
33%+MinimalGrade II
33%-Diffuse focal or thickGrade III
40%+Diffuse focal or thickGrade IV
Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified
Fisher Scale." Neurosurgery 59.1 (2006): 21-27.

Fisher, CM, Kistler, JP, Davis, JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by CT scanning. Neurosurgery 1980;
6:1.
Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified Fisher
Scale." Neurosurgery 59.1 (2006): 21-27.

Ageing blood on MRI
The imaging characteristics of blood on MRI are variable and change with the
age of the blood.
In general, five stages of haematoma evolution are recognised:
isointense on T1
isointense to hyperintense on T2
1- Hyperacute
T2 signal intensity drops (T2 shortening)
T1 remains intermediate-to-long
2- Acute (1-2 days)
T1 signal gradually increases (T1
shortening) to become hyperintense
3- Early subacute (2-7days)
increase in T2 signal4- Late subacute (7-14days)
low on both T1 and T25- Chronic (>14-28 days)

Exapmple to Subacute ICH in MRI

Hemostasis and Coagulopathy, Antiplatelet Agents,
and DVT Prophylaxis
1. Patients with a severe coagulation factor deficiency or severe
thrombocytopenia should receive appropriate factor replacement therapy or
platelets, respectively (Class I; Level of Evidence C).
2. Patients with ICH whose INR is elevated because of VKA should have their
VKA withheld, receive therapy to replace vitamin K–dependent factors and
correct the INR, and receive intravenous vitamin K (Class I; Level of
Evidence C). PCCs may have fewer complications and correct the INR
more rapidly than FFP and might be considered over FFP (Class IIb; Level
of Evidence B). rFVIIa does not replace all clotting factors, and although the
INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is
not recommended for VKA reversal in ICH (Class III; Level of Evidence C).

and DVT Prophylaxis
3. For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban,
treatment with FEIBA, other PCCs, or rFVIIa might be considered on an
individual basis. Activated charcoal might be used if the most recent dose of
dabigatran, apixaban, or rivaroxaban was taken <2 hours earlier.
Hemodialysis might be considered for dabigatran (Class IIb; Level of
Evidence C).
4. Protamine sulfate may be considered to reverse heparin in patients with
acute ICH (Class IIb; Level of Evidence C).
5. The usefulness of platelet transfusions in ICH patients with a history of
antiplatelet use is uncertain (Class IIb; Level of Evidence C).
6. Although rFVIIa can limit the extent of hematoma expansion in
noncoagulopathic ICH patients, there is an increase in thromboembolic risk
with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa
is not recommended (Class III; Level of Evidence A). It was also not
recommended by ESO, 2010
Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.

and DVT Prophylaxis
7. Patients with ICH should have intermittent pneumatic compression for
prevention of venous thromboembolism beginning the day of hospital
admission (Class I; Level of Evidence A). Graduated compression
stockings are not beneficial to reduce DVT or improve outcome (Class III;
8. After documentation of cessation of bleeding, low dose subcutaneous low-
molecular-weight heparin or unfractionated heparin may be considered for
prevention of venous thromboembolism in patients with lack of mobility after
1 to 4 days from onset (Class IIb; Level of Evidence B).
9. Systemic anticoagulation or IVC filter placement is probably indicated in ICH
patients with symptomatic DVT or PE (Class IIa; Level of Evidence C).
The decision between these 2 options should take into account several factors,
including time from hemorrhage onset, hematoma stability, cause of
hemorrhage, and overall patient condition (Class IIa; Level of Evidence C).

and DVT Prophylaxis

management dilemma
Hemorrhagic stroke
The conflict1
:
(1) Severe elevations in BP may worsen ICH.
(2) Enlargement of the hematoma is associated with neurologic deterioration and
worse outcomes. These observations indicate that significant improvements in
patient outcome from ICH can be achieved by minimizing hematoma
enlargement.
1- Stroke 2007; 38:1072–1075.

The guidelines:
For ICH patients presenting with SBP between 150 and 220 mm Hg and without
contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe
(Class I; Level of Evidence A) and can be effective for improving functional
outcome (Class IIa; Level of Evidence B).
For ICH patients presenting with SBP >220 mmHg, it may be reasonable to
consider aggressive reduction of BP with a continuous intravenous infusion and
frequent BP monitoring (Class IIb; Level of Evidence C).
This is also supported by European Stroke Organisation (ESO) guidelines in 2014
who recommends In acute ICH within 6 h of onset, intensive blood pressure
reduction (systolic target <140 mmHg in <1 h) is safe and may be superior to a
systolic target <180 mmHg. No specific agent can be recommended.
Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.

Studies have been carried out in that respect:
(1) In a randomized controlled trial [INTensive Blood Pressure Reduction in Acute
Cerebral Hemorrhage trial (INTERACT1)]1 on 404 patients with acute
spontaneous ICH, intensive BP lowering treatment (target SBP 140 mmHg),
compared with traditional management (target SBP 180 mmHg), was associated
with a reduction in hematoma growth at 24 h (14 vs. 26%). The study showed
that SBP greater than 140–150 mmHg within 12 h of ICH is associated with more
than double the risk of subsequent death or dependency. Most recently, the main
phase [(INTERACT2)]2 trial has shown no increase in death or serious adverse
events from early intensive BP lowering in eligible patients with elevated SBP.1
(2) The Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial
further confirmed these findings.3
1- Stroke. 2012;43:2236–2238. 2- N Engl J Med. 2013;368:2355–2365. 3- Neurocrit Care 2007; 6:56–66.

Louis Pasteur
French chemist and microbiologist

Treatment (cont.)
Factors Recommendation
General
Monitoring and
Nursing
Initial monitoring and management of ICH patients should take
place in an intensive care unit or dedicated stroke unit with physician
and nursing neuroscience acute care expertise (Class I; Level of
Evidence B).
Airway
&Breathing
Supplemental oxygen should be provided to maintain
oxygen saturation >94% (Class I; Level of Evidence C).
Supplemental oxygen is not recommended in nonhypoxic patients
with acute ischemic stroke (Class III; Level of Evidence B).
Mobilization Early mobilization of less severely affected patients and measures
to prevent subacute complications of stroke are recommended
(Class I; Level of Evidence C).
Nutrition A formal screening procedure for dysphagia should be performed
in all patients before the initiation of oral intake to reduce the risk of
pneumonia (Class I; Level of Evidence B).
Insert a nasogastric tube if the patient fails the swallow test.
Consider PEG only if prolonged enteral feeding is required (Class
I; Level of Evidence B).
Stroke. 2015; 46: 3020-3035

Infection and
fever
Treatment of fever after ICH may be reasonable (Class IIb; Level of
Evidence C).
Sources of hyperthermia (temperature >38°C) should be identified and
treated, and antipyretic medications should be administered to lower
temperature in hyperthermic patients with stroke (Class I; Level of
Evidence C).
Routine use of prophylactic antibiotics has not been shown to be
Patients with suspected pneumonia or urinary tract infections should be
treated with appropriate antibiotics (Class I; Level of Evidence A).
Seizures Clinical as well as EEG documented seizures should be treated with
antiseizure drugs (Class I; Level of Evidence A).
Prophylactic antiseizure medication is not recommended (Class III;
Blood
Glucose
Glucose should be monitored. Both hyperglycemia and hypoglycemia
should be avoided (Class I; Level of Evidence C).
Treatment (cont.)

Prolonged
recumbency
As regard ICH, After documentation of cessation of bleeding, lowdose
subcutaneous low-molecular-weight heparin or unfractionated heparin
may be considered for prevention of venous thromboembolism in
patients with lack of mobility after 1 to 4 days from onset (Class IIb;
Patients with ICH should have intermittent pneumatic compression for
prevention of venous thromboembolism beginning the day of hospital
admission (Class I; Level of Evidence A).
Brain
dehydratin
measures
Corticosteroids should not be administered for treatment of elevated
ICP in ICH (Class III; Level of Evidence B). In agreement with
International stroke foundation guidelines, 2010 (A)
Treatment (cont.)

Prevention of Recurrent ICH
1. BP should be controlled in all ICH patients (Class I; Level of Evidence
A). Measures to control BP should begin immediately after ICH onset
(Class I; Level of Evidence A). A long-term goal of BP <130 mmHg
systolic and 80 mmHg diastolic is reasonable (Class IIa; Level of
Evidence B).
2. Lifestyle modifications, including avoidance of alcohol use greater than 2
drinks per day, tobacco use, and illicit drug use, as well as treatment of
obstructive sleep apnea, are probably beneficial (Class IIa; Level of
Evidence B).
3. Avoidance of long-term anticoagulation with warfarin as a treatment for
nonvalvular atrial fibrillation is probably recommended after warfarin-
associated spontaneous lobar ICH because of the relatively high risk of
recurrence (Class IIa; Level of Evidence B).

Prevention of Recurrent ICH
4. The optimal timing to resume oral anticoagulation after anticoagulant-
related ICH is uncertain. Avoidance of oral anticoagulation for at least 4
weeks, in patients without mechanical heart valves, might decrease the
risk of ICH recurrence (Class IIb; Level of Evidence B). If indicated,
aspirin monotherapy can probably be restarted in the days after ICH,
although the optimal timing is uncertain (Class IIa; Level of Evidence B).
5. The usefulness of dabigatran, rivaroxaban, or apixaban in patients with
atrial fibrillation and past ICH to decrease the risk of recurrence is
uncertain (Class IIb; Level of Evidence C).
6. There are insufficient data to recommend restrictions on the use of statins
in ICH patients (Class IIb; Level of Evidence C).

Statins and ICH
There are conflicting reports regarding the use of statins in patients with ICH.
Stroke Prevention With Aggressive Reduction in Cholesterol Levels (SPARCL)
study, the benefit of high-dose atorvastatin in reducing recurrent ischemic stroke
was offset in part by an increased risk of ICH. However it was non significant.
Also a study in 2012 over 163 patients with ICH 40 was on statin treatment,
published in Stroke journal concluded that Statin use in patients with ICH is
independently associated with microbleeds
However another metanalysis in 2013, studied 31 randomized controlled trials
that included 91 588 statin-treated patients found no significant association
between statin use and ICH (OR, 1.08; 95% CI, 0.88–1.32; P=0.47).
It remains unclear whether statins should be continued or discontinued in ICH
patients.
Stroke. 2012;43:2677-2681
Neurology. 2008;70(24 Pt 2):2364–2370.
Stroke.2012;43:2149–2156.

By the year 2000 the commonest killers such
as coronary heart disease, stroke, respiratory,
diseases and many cancers will be wiped out.
Anonymous
Irish Times (24 Apr 1987)

1- Primary Prevention
FACTORS RECOMMENDATION
Physical activity Physical activity is recommended because it is associated
with a reduction in the risk of stroke (Class I; Level of
Evidence B).
Diet Reduced intake of sodium and increased intake of potassium
as indicated in the US Dietary Guidelines for Americans are
recommended to lower BP (Class I; Level of Evidence A).
A DASH-style diet, which emphasizes fruits, vegetables, and
low-fat dairy products and reduced saturated fat, is
recommended to lower BP127,218 (Class I; Level of Evidence
A).
Hypertension Annual screening for high BP and health-promoting lifestyle
modification are recommended for patients with prehypertension
(SBP of 120 to 139 mmHg or DBP of 80 to 89 mmHg) (Class I;
Patients who have hypertension should be treated with
antihypertensive drugs to a target BP of <140/90 mm Hg (Class
I; Level of Evidence A).
Stroke. 2014;45:3754–3832.

1- Primary Prevention (cont.)
Dyslipidemia In addition to therapeutic lifestyle changes, treatment with an
HMG coenzyme-A reductase inhibitor (statin) medication is
recommended for the primary prevention of ischemic stroke in
patients estimated to have a high 10-year risk for cardiovascular
events as recommended (Class I; Level of Evidence A).
Obesity Among overweight (BMI=25 to 29 kg/m2) and obese (BMI >30
kg/m2) individuals, weight reduction is recommended for
lowering BP and reducing the risk of stroke (Class I; Level of
Evidence A).
Diabetes mellitus Control of BP in accordance with guidelines to a target of
<140/90 mm Hg is recommended in patients with type 1 or type
2 diabetes mellitus (Class I; Level of Evidence A).
Treatment of adults with diabetes mellitus with a statin,
especially those with additional risk factors, is recommended to
lower the risk of first stroke (Class I; Level of Evidence A).
Smoking Cessation of smoking.
Stroke. 2014;45:3754–3832.

1- Primary Prevention (cont.)
AF For patients with valvular AF at high risk for stroke, defined as a
CHA 2DS2-VASc score of ≥2 and acceptably low risk for
hemorrhagic complications, long-term oral anticoagulant therapy
with warfarin at a target INR of 2.0 to 3.0 is recommended (Class I;
For patients with nonvalvular AF, a CHA2DS2-VASc score of ≥2,
and acceptably low risk for hemorrhagic complications, oral
anticoagulants are recommended (Class I). Options include warfarin
(INR, 2.0 to 3.0) (Level of Evidence A), dabigatran (Level of
Evidence B), apixaban (Level of Evidence B), and rivaroxaban
(Level of Evidence B).
Alcohol Reduction or elimination of alcohol consumption in
heavy drinkers (Class I; Level of Evidence A).
Prophylactic
aspirin !
Aspirin is not useful for preventing a first stroke in lowrisk
individuals (Class III; Level of Evidence A).
 Aspirin is not useful for preventing a first stroke in people with
diabetes mellitus in the absence of other highrisk conditions (Class
III; Level of Evidence A).
Stroke. 2014;45:3754–3832.

Primary Prevention (cont.)
CHADS2 and CHA2DS2 VASc

HAS BLED score
HAS-BLED categorizes those into low (score 0-2) or high (≥3) risk, where the
latter can be identified for more regular review and follow-up.

SAMe-TT2R2 Score
b= Two of the following: hypertension, diabetes mellitus, coronary artery disease
or myocardial infarctions, peripheral artery disease, congestive heart failure,
previous stroke, pulmonary disease, or hepatic or renal disease.

SAMe-TT2R2 Score
 The SAMe-TT2R2 score is proposed as a means to help with decision making,
to identify those newly diagnosed nonanticoagulated AF patients who have a
probability of doing well while taking a vitamin K antagonist (VKA) (with SAMe-
TT 2R2 score, 0-2) and achieve a time in therapeutic range (TTR) of at least
65% or 70%.
 In contrast, a SAMe-TT2R2 score of more than 2 suggests that such patients
are unlikely to achieve a good TTR while taking a VKA, and a non-VKA oral
anticoagulant should be used upfront, without a “trial of warfarin” period.

Jacobson et al. Journal of Clinical Lipidology (2014) 8, 473–488

SPRINT trial
The SPRINT Research Group N Engl J Med 2015; 373:2103-2116
9361 persons was randomly assigned were at least 50 years old with a
systolic blood pressure of 130 mm Hg or higher (180 mmHg) and an
increased cardiovascular risk, but without diabetes, to a systolic blood-
pressure target of less than 120 mm Hg (intensive treatment) or a target of
less than 140 mm Hg (standard treatment).

SPRINT trial (cont.)
All participants had at least 1 other significant cardiovascular
risk factor, including chronic kidney disease; age 75 years or
older; a previous cardiovascular event (except stroke); or an
elevated cardiovascular risk based on their Framingham risk
score.

The primary composite outcome was myocardial infarction,
other acute coronary syndromes, stroke, heart failure, or death
from cardiovascular causes. (Funded by the National Institutes
of Health; ClinicalTrials.gov

The mean baseline blood pressure among all
participants was 139.7/78.1 mm Hg.
Mean blood pressure values at 1 year into the
study were 121.4/68.7 mm Hg in the intensive
treatment group and 136.2/76.3 mm Hg in the
standard treatment group.
1- ClinicalTrials.gov. Systolic Blood Pressure Intervention Trial (SPRINT).
https://clinicaltrials.gov/ct2/show/NCT01206062?term=Systolic+Blood+Pressure+Intervention+Trial&rank=1. Accessed November 9,
2015.

The intervention was stopped early after a median
follow-up of 3.26 years in stead of December
2018 which was the Estimated Study Completion
Date1
1- ClinicalTrials.gov. Systolic Blood Pressure Intervention Trial (SPRINT).
https://clinicaltrials.gov/ct2/show/NCT01206062?term=Systolic+Blood+Pressure+Intervention+Trial&rank=1. Accessed November 9,
2015.

 The lower target group of less than 120 mm Hg systolic
blood pressure had a 25% lower relative risk for the primary
composite end point of myocardial infarction, acute coronary
syndrome, stroke, acute decompensated heart failure, and
cardiovascular death vs the group with a target of less than
140 mm Hg.

 In addition, the lower-target group had 27% lower risk for
all-cause mortality and 43% lower risk for cardiovascular
death. However, this group also had higher adverse events
such as hypotension, syncope, and acute kidney injury or
kidney failure.

Rates of serious adverse events of hypotension,
syncope, electrolyte abnormalities, and acute
kidney injury or failure, but not of injurious falls,
were higher in the intensive-treatment group than in
the standard-treatment group.

CONCLUSIONS
Among patients at high risk for cardiovascular events but
without diabetes, targeting a systolic blood pressure of less
than 120 mm Hg, as compared with less than 140 mm Hg,
resulted in lower rates of fatal and nonfatal major
cardiovascular events and death from any cause, although
significantly higher rates of some adverse events were
observed in the intensive-treatment group.

Dr Marc Pfeffer (Harvard Medical School, Boston, MA)
CAUTIONS AS REGARD STUDY
A lot of effort is required to hit this target, including initial combination therapy
and frequent office visits “marathon effort”.
Excluding diabetics is "a black hole" in the study and limits its applicability.
Only approximately half of adults achieve a blood pressure of 140 mm Hg or
less, as consistent with current recommendations.
“Physicians "shouldn't expect a 'thank you' from patients
when you add another pill to reduce their blood pressure.“1

Alfred Nobel
Swedish chemist, engineer, innovator, and
armaments manufacturer. He was the
inventor of dynamite.

3- Secondary Prevention
The major treatable atherosclerotic risk factors for stroke are the following:
●Hypertension
●Diabetes mellitus
●Smoking
●Dyslipidemia
Factors
Treatment
Recommendations
Hypertension
Initiation of BP therapy is indicated for previously untreated patients
with ischemic stroke or TIA who, after the first several days, have an
established BP ≥140 mm Hg systolic or ≥90 mm Hg diastolic (Class I;
Resumption of BP therapy is indicated for previously treated patients
with known hypertension for both prevention of recurrent stroke and
prevention of other vascular events in those who have had an ischemic
stroke or TIA and are beyond the first several days (Class I; Level of
Evidence A).
ASA/AHA. Stroke. 2014; 45: 2160-2236

3- Secondary Prevention (cont.)
Factors
Treatment
Recommendations
Hypertension
(cont.)
Goals for target BP level or reduction from pretreatment baseline
are uncertain and should be individualized, but it is reasonable to
achieve a systolic pressure <140 mm Hg and a diastolic pressure
<90 mm Hg (Class IIa; Level of Evidence B).
For patients with a recent lacunar stroke, it might be reasonable
to target a systolic BP of <130 mm Hg (Class IIb; Level of
Evidence B).
Glucose
disorders
After a TIA or ischemic stroke, all patients should probably be
screened for DM with testing of fasting plasma glucose, HbA1c, or
an oral glucose tolerance test. (Class IIa; Level of Evidence C).
Use of existing guidelines from the ADA for glycemic control and
cardiovascular risk factor management is recommended for
patients with an ischemic stroke or TIA who also have DM or pre-
DM (Class I; Level of Evidence B).

Factors
Treatment
Recommendations
Dyslipidemia Statin therapy with intensive lipid-lowering effects is recommended to
reduce risk of stroke and cardiovascular events among patients with
ischemic stroke or TIA presumed to be of atherosclerotic origin and an
LDL-C level ≥100 mg/dL with or without evidence for other
ASCVD (Class I; Level of Evidence B).
Statin therapy with intensive lipid-lowering effects is recommended to
reduce risk of stroke and cardiovascular events among patients with
ischemic stroke or TIA presumed to be of atherosclerotic origin, an
LDL-C level <100 mg/dL, and no evidence for other clinical
ASCVD (Class I; Level of Evidence C).
Obesity All patients with TIA or stroke should be screened for obesity with
measurement of BMI (Class I; Level of Evidence C).
Smoking Healthcare providers should strongly advise every patient with stroke
or TIA who has smoked in the past year to quit (Class I; Level of
Evidence C).
It is reasonable to advise patients after TIA or ischemic stroke to avoid
environmental (passive) tobacco smoke (Class IIa; Level of Evidence
B).

Factors
Treatment
Recommendations
Intracranial
atherosclero
sis
For patients with recent stroke or TIA (within 30 days) attributable to severe
stenosis (70%–99%) of a major intracranial artery, the addition of clopidogrel
75 mg/d to aspirin for 90 days might be reasonable(Class IIb; Level of
Evidence B).
For patients with a stroke or TIA attributable to 50% to 99% stenosis of a
major intracranial artery, maintenance of systolic BP below 140 mm Hg and
high-intensity statin therapy are recommended(Class I; Level of Evidence
B).
AF For patients who have experienced an acute ischemic stroke or TIA with no
other apparent cause, prolonged rhythm monitoring (≈30 days) for AF is
reasonable within 6 months of the index event (Class IIa; Level of Evidence
C).
VKA therapy (Class I; Level of Evidence A), apixaban (Class I; Level of
Evidence A), and dabigatran (Class I; Level of Evidence B) are all indicated
for the prevention of recurrent stroke in patients with nonvalvular AF, whether
paroxysmal or permanent.

Factors
Treatment
Recommendations
AF (cont.)
Rivaroxaban is reasonable for the prevention of recurrent stroke in
patients with nonvalvular AF (Class IIa; Level of Evidence B).
For patients with ischemic stroke or TIA and AF who are unable to take
oral anticoagulants, aspirin alone is recommended (Class I; Level of
Evidence A). The addition of clopidogrel to aspirin therapy, compared with
aspirin therapy alone, might be reasonable (Class IIb; Level of Evidence
B).
For most patients with a stroke or TIA in the setting of AF, it is
reasonable to initiate oral anticoagulation within 14 days after the onset of
neurological symptoms (Class IIa; Level of Evidence B).
In the presence of high risk for hemorrhagic conversion (ie, large infarct,
hemorrhagic transformation on initial imaging, uncontrolled hypertension,
or hemorrhage tendency), it is reasonable to delay initiation of oral
anticoagulation beyond 14 days (Class IIa; Level of Evidence B).

Factors
Treatment
Recommendations
Extracranial
astheroscler
osis
For patients with a TIA or ischemic stroke within the past 6 months and
ipsilateral severe (70%–99%) carotid artery stenosis as documented by
noninvasive imaging, carotid endartrectomy (CEA) is recommended if the
perioperative morbidity and mortality risk is estimated to be <6% (Class I;
For patients with recent TIA or ischemic stroke and ipsilateral moderate
(50%–69%) carotid stenosis as documented by catheter-based imaging or
noninvasive imaging with corroboration (eg, magnetic resonance
angiogram or computed tomography angiogram), CEA is recommended
depending on patient-specific factors, such as age, sex, and comorbidities
When the degree of stenosis is <50%, CEA and CAS are not
recommended (Class III; Level of Evidence A).
Optimal medical therapy, which should include antiplatelet therapy, statin
therapy, and risk factor modification, is recommended for all patients with
carotid artery stenosis(Class I; Level of Evidence A).

Factors
Treatment
Recommendations
Antiplatelet
For patients with noncardioembolic ischemic stroke or TIA, the use of
antiplatelet agents rather than oral anticoagulation is recommended to
reduce the risk of recurrent stroke and other cardiovascular events (Class
Aspirin (50–325 mg/d) monotherapy (Class I; Level of Evidence A) or
the combination of aspirin 25 mg and extended-release dipyridamole 200
mg twice daily (Class I; Level of Evidence B) is indicated as initial
therapy after TIA or ischemic stroke for prevention of future stroke.
Clopidogrel (75 mg) monotherapy is a reasonable option for secondary
prevention of stroke in place of aspirin or combination aspirin/dipyridamole
(Class IIa; Level of Evidence B).
The combination of aspirin and clopidogrel might be considered for
initiation within 24 hours of a minor ischemic stroke or TIA and for
continuation for 21 days (Class IIb; Level of Evidence B).

Factors
Treatment
Recommendations
Antiplatelet
The combination of aspirin and clopidogrel, when initiated days to years
after a minor stroke or TIA and continued for 2 to 3 years, increases the
risk of hemorrhage relative to either agent alone and is not recommended
for routine long-term secondary prevention after ischemic stroke or TIA
(Class III; Level of Evidence A).
For patients with noncardioembolic ischemic stroke or TIA, the use of
antiplatelet agents rather than oral anticoagulation is recommended to
reduce the risk of recurrent stroke and other cardiovascular events (Class

Factors
Treatment
National Stroke Foundation Guidelines, 2010
Antiplatelet
(cont.)
Long-term antiplatelet therapy should be prescribed to all people with
ischaemic stroke or TIA who are not prescribed anticoagulation therapy
(A).
Low-dose aspirin and modified release dipyridamole or clopidogrel alone
should be prescribed to all people with ischaemic stroke or TIA, taking into
consideration patient co-morbidities (A)
Aspirin alone can be used, particularly in people who do not tolerate
aspirin plus dipyridamole or clopidogrel (A).
The combination of aspirin plus clopidogrel is not recommended for the
secondary prevention of cerebrovascular disease in people who do not
have acute coronary disease or recent coronary stent (A).

Treatment (cont.)
Known Factors That Cause Stroke Progression
• Hypotension
• Hyperglycemia
• Hyperthermia
• Infection
• Cerebral hypoperfusion
These factors affect penumbra………………

ACS vs. Stroke
The success of thrombolytic therapy in coronary occlusive syndromes
created high expectations for thrombolytic therapy in acute, ischemic stroke,
and these expectations prompted a massive effort to create “stroke centers”
in major hospitals, each with a “stroke team” to direct the management of
acute stroke. The following is an accounting of what this effort has
accomplished:
Number of strokes each year in the United States 700,0001
Number of ischemic strokes (88% ) 616,000
Number of stroke patients who receive lytic therapy (2%) 12,320
Number of patients who benefit from lytic therapy (1 in 9) 1,369
% of strokes that benefit from lytic therapy (1369/700,000) 0.2%
True Story….
1- Mozzafarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics—2015 update: a report from the
American Heart Association.Circulation. 2015:e29–322.

Overall Bottom Line
Remember
• “Time is brain”
• Stroke awareness: health care team, info for everyone
• Common mistakes may lead to fatal consequences
• “There is no Stroke Motel”: Patients will receive best care; if
length of stay shortened

Yasser Arafat
Palestinian leader
Died on 11 November 2004 at the age of 75 of
what French doctors called a massive
hemorrhagic cerebrovascular accident
(hemorrhagic stroke).

Stroke guidelines, 2015

Empfohlen

Empfohlen

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (20)

Ähnlich wie Stroke guidelines, 2015

Ähnlich wie Stroke guidelines, 2015 (20)

Mehr von Usama Ragab

Mehr von Usama Ragab (20)

Kürzlich hochgeladen

Kürzlich hochgeladen (20)

Stroke guidelines, 2015