Update in managment of cerebrovascular accident

1. Management of
cerebrovascular accident
Dr. HAIFA ALSHWIKH

2. Initial assessment and management of acute
stroke
— The management of patients who have had an ischemic
stroke involves several phases. The goals in the initial phase
include:
-Insuring medical stability
-Quickly reversing any conditions that are contributing to the
symptoms
-Uncovering the pathophysiologic basis of the neurologic
symptoms
-Screening for potential contraindications to thrombolysis
-Diagnosing hemorrhage

3. Diagnosing an intracerebral hemorrhage (ICH) or subarachnoid
hemorrhage (SAH) as soon as possible can be lifesaving
The history may be helpful in this regard. The presence of onset
headache and vomiting favor the diagnosis of ICH or SAH compared
with a thromboembolic stroke , while the abrupt onset of impaired
cerebral function without focal symptoms favors the diagnosis of
SAH.
Even with these clues, diagnosing intracranial hemorrhage on clinical
grounds is very imprecise, so early triage of the patient to CT or MRI
scan is critical. However, it is important to assess and optimize vital
physiologic function before sending the patient for an imaging study.

4. The frequency of sentinel headache, onset headache, and vomiting in
three subtypes of stroke: subarachnoid hemorrhage (SAH),
intraparenchymal (intracerebral) hemorrhage (IPH), and ischemic stroke
(IS). Onset headache was present in virtually all patients with SAH and
about one-half of those with IPH; all of these symptoms were infrequent in

5. History and physical —
The history and physical examination should be used to distinguish
between other disorders in the differential diagnosis of brain ischemia
As examples, seizures, syncope, migraine, and hypoglycemia can
mimic acute ischemia.
The most difficult cases involve patients with focal signs and altered
level of consciousness. It is important to ask the patient or a relative
whether the patient takes insulin or oral hypoglycemic agents, has a
history of a seizure disorder or drug overdose or abuse, medications on
admission, or recent trauma
The physical examination should include careful evaluation of the neck
and retroorbital regions for vascular bruits, and palpation of pulses in the
neck, arms, and legs to assess for their absence, asymmetry, or
irregular rate. The heart should be auscultated for murmurs,
Fluctuations in blood pressure occasionally precede fluctuations in
clinical signs.
.

6. The skin should be examined for signs of endocarditis, cholesterol
emboli, purpura, or ecchymoses.
The funduscopic examination may be helpful if there are cholesterol
emboli or papilledema. The head should be examined for signs of
trauma. A tongue laceration may occur with tongue biting during a
seizure.
The neck should be immobilized until evaluated radiographically for
evidence of serious trauma if there is a report or suspicion of a fall.
Examination of the extremities is important to detect deep vein
thrombosis, which can cause systemic embolization in patients with a
patent foramen ovale, and to look for evidence of systemic arterial
emboli from other sources

7. Airway and breathing — Patients with increased intracranial
pressure due to hemorrhage, vertebrobasilar ischemia, or
bihemispheric ischemia can present with a decreased respiratory drive
or muscular airway obstruction. Hypoventilation, with a resulting
increase in carbon dioxide, may lead to cerebral vasodilation, which
further elevates intracranial pressure.
Intubation may be necessary to restore adequate ventilation and to
protect the airway from aspiration; this is especially important in the
presence of vomiting, which occurs commonly with increased
intracranial pressure, vertebrobasilar ischemia, and intracranial
hemorrhage.
Patients with adequate ventilation should have the oxygen saturation
monitored.
Patients who are hypoxic should receive supplemental oxygen.

8. Dysphagia and aspiration — Dysphagia is common after
stroke and is a major risk factor for developing aspiration
pneumonia. It is important to assess swallowing function prior
to administering oral medications or food. Thus, prevention of
aspiration in patients with acute stroke includes initial nulla per
os (NPO) status until swallowing function is evaluated.
Head position — During the acute phase of stroke, the head
of bed position should be individualized with respect to the risk
of elevated intracranial pressure and aspiration, and the
presence of comorbid cardiopulmonary disease. However,
available data are limited, and no randomized trials have
addressed these issues

9. We recommend keeping the head in neutral alignment with the
body and elevating the head of the bed to 30 degrees for all
patients in the acute phase of stroke who are at risk for any of
the following problems:
Elevated intracranial pressure (eg, with large ischemic stroke,
intracerebral hemorrhage, space-occupying lesion, or other
cause of elevated intracranial pressure) ,Aspiration (eg, those
with dysphagia and/or diminished consciousness)
,Cardiopulmonary decompensation or oxygen desaturation
(eg, those with chronic cardiac and pulmonary disease)
We suggest keeping the head of bed flat (0 to 15 degree head-
of-bed position) for patients in the acute phase of stroke who
are not at risk for elevated intracranial pressure, aspiration, or
worsening cardiopulmonary status.

10. Immediate laboratory studies —
Emergent brain imaging with CT or MRI is mandatory in all patients
with sudden neurologic deterioration or acute stroke.
All patients with suspected stroke should have the following studies
immediately upon admission to the emergency department.
-Noncontrast brain CT or brain MRI
-Electrocardiogram
-Complete blood count including platelets
-Cardiac enzymes and troponin
-Electrolytes, urea nitrogen, creatinine
-Serum glucose
-Prothrombin time and international normalized ratio (INR)Partial
thromboplastin time
-Oxygen saturation
-Lipid profile

11. The following laboratory studies are appropriate in selected patients
Liver function tests
Toxicology screen
Blood alcohol level
Pregnancy test in women of child-bearing
potentialArterial blood gas if hypoxia is suspected
Lumbar puncture if subarachnoid hemorrhage is suspected and head
CT scan is negative for blood
Electroencephalogram if seizures are suspected

12. HYPERCOAGULABLE PROFILE
PATIENTS < 55 YEARS OLD
CBC w/ diff &
platelets
PT/aPTT
Fibrinogen
Factor VIII
Factor VII
C-reactive
protein
Antithrombin III
Protein C
Protein S (total
& free)
Lipoprotein

13. Activated protein C resistance (APCR) (& Leiden factor V
mutation if
Prothrombin mutation
Antiphospholipid antibodies
Lupus anticoagulant
Anticardiolipin abs
Anti-β-2-glycoprotein I abs
Antiphosphatidylserine abs
Methyltetrahydrofolatereductase (MTHFR mutations
Sickle cell screen

14. Hyperglycemia — Hyperglycemia, generally defined as a blood
glucose level >126 mg/dL (>7.0 mmol/L), is common in patients
with acute ischemic stroke and is associated with poor functional
outcome , In a series of 59 patients with acute ischemic stroke,
admission hyperglycemia was present in 32 percent of patients
without diabetes and 81 percent of patients with diabetes ,
Stress hyperglycemia may be the most common cause ,
although newly diagnosed diabetes is also important
Hyperglycemia may augment brain injury by several
mechanisms including increased tissue acidosis from anaerobic
metabolism, free radical generation, and increased blood brain
barrier permeability. Several lines of evidence point to the
deleterious effects of elevated glucose in acute stroke

15. Hypoglycemia —
Hypoglycemia can cause focal neurologic deficits mimicking stroke,
and severe hypoglycemia alone can cause neuronal injury. It is
important to check the blood sugar and rapidly correct low serum
glucose at the first opportunity.
Normoglycemia is the desired goal while avoiding marked elevation of
serum glucose . It may be reasonable to administer glucose
immediately after drawing a blood sample in "stroke" patients known
to take insulin or oral hypoglycemic agents.

16. Fever — Fever has special significance in patients presenting
with acute neurologic deterioration.
may occur in patients with a primary central nervous system infection
such as meningitis, subdural empyema, brain abscess, and infective
endocarditis. These conditions need to be excluded as the etiology of
fever. In addition, common etiologies of fever including aspiration
pneumonia and urinary tract infection should also be excluded.
Fever may contribute to brain injury in patients with an acute stroke..
Hyperthermia may act via several mechanisms to worsen cerebral
ischemia ,Enhanced release of neurotransmitters, Exaggerated
oxygen radical production, More extensive blood-brain barrier
breakdown, enhanced inhibition of protein kinases, Worsening of
cytoskeletal proteolysis
The source of fever should be investigated and treated, and
antipyretics should be used to lower temperature in febrile patients
with acute stroke. We suggest maintaining normothermia for at least
the first several days after an acute stroke

17. BLOOD PRESSURE MANAGEMENT IN CVA
— In patients with ischemic stroke, the perfusion pressure distal to the
obstructed vessel is low, and the distal vessels are dilated. Blood flow in
these dilated vessels is thought to be dependent upon the systemic blood
pressure.
The arterial blood pressure is usually elevated in patients with an acute
stroke. This may be due to chronic hypertension, an acute sympathetic
response, or to other stroke-mediated mechanisms ,In many cases,
however, the acutely elevated blood pressure is necessary to maintain
brain perfusion. A neuroimaging study with CT or MRI is critical to help
guide blood pressure therapy in stroke patients.
The observation that the blood pressure frequently rises spontaneously
following cerebral ischemia is consistent with this protective hypothesis,
although a stress response to the acute event and to hospitalization may
also contribute
The hypertensive effect is transient, as blood pressure falls by as much as
20/10 mmHg within 10 days.

18. Blood pressure recommendations —
Ischemic stroke:
Most consensus guidelines recommend that blood pressure NOT be
treated acutely in the patient with ischemic stroke unless the
hypertension is extreme (systolic blood pressure >220 mmHg or
diastolic blood pressure >120 mmHg), or the patient has active ischemic
coronary disease, heart failure, aortic dissection, hypertensive
encephalopathy, acute renal failure, or pre-eclampsia/eclampsia]
When treatment is indicated, cautious lowering of blood pressure by
approximately 15 percent during the first 24 hours after stroke onset is
suggested .
Blood pressure management in acute stroke remains controversial.
Guidelines from the American Heart Association/American Stroke
Association published in 2007 suggest that antihypertensive medications
should be restarted at approximately 24 hours after stroke onset in
patients with preexisting hypertension who are neurologically stable,
unless a specific contraindication to restarting treatment is known

19. However, patients with extracranial or intracranial stenoses may
require a slower reduction in blood pressure (eg, over seven to ten
days after ischemic stroke), as some degree of blood pressure
elevation may be necessary to maintain cerebral blood flow to
ischemic brain regions.
If pharmacologic therapy is given, intravenous labetalol is generally
the drug of choice.
Special considerations apply to blood pressure control in patients with
ischemic stroke who are eligible for thrombolytic therapy. Before lytic
therapy is started, treatment is recommended so that systolic blood
pressure is ≤185 mmHg and diastolic blood pressure is ≤110 mmHg
The blood pressure should be stabilized and maintained below
180/10mmHg for at least 24 hours after intravenous tPA treatment.

20. Text of guidelines state “Do not Rx unless BP >
220/120,” but also state:
◦No data to suggest 220/120 is dangerous & requires Rx
◦Evidence that BP lowering worsens outcomes is
concerning
◦Goal is to avoid overtreating pts until definitive data
available
Only definite indications to  BP emergently in
AIS:
◦AMI, CHF, Ao dissection, ARF, or HTN encephalopathy
◦Candidate for thrombolysis and BP > 185/110

21. Intracranial hemorrhage —
In both intracerebral hemorrhage (ICH) and subarachnoid
hemorrhage (SAH), the approach to blood pressure management must
take into account the potential benefits (eg, reducing further bleeding)
and risks (eg, reducing cerebral perfusion) of blood pressure lowering:
Reducing the blood pressure in patients with either ICH or SAH may be
beneficial by minimizing further bleeding and continued vascular damage
Patients with an intracranial hemorrhage due to ICH or SAH may have
increased intracranial pressure (ICP) due to blood within the cranium.
Cerebral perfusion pressure (CPP) equals MAP minus ICP. Thus,
increases in MAP may be the only means to maintain CPP above 60 to
70 mmHg, the level necessary to maintain perfusion
MAP=Diastolic P+1/3( Systolic P- Diastolic P)

22. Guidelines — Current guidelines for managing elevated blood
pressure in acute spontaneous ICH are as follows:
For patients with SBP >200 mmHg or MAP >150 mmHg, consider
aggressive reduction of blood pressure with continuous intravenous
infusion of medication accompanied by frequent (every five minutes)
blood pressure monitoring
For patients with SBP >180 mmHg or MAP >130 mmHg and evidence
or suspicion of elevated ICP, consider monitoring ICP and reducing
blood pressure using intermittent or continuous intravenous medication
to keep cerebral perfusion pressure in the range of 61 to 80 mmHg
For patients with SBP >180 mmHg or MAP >130 mmHg and
no evidence or suspicion of elevated ICP, consider a modest reduction
of blood pressure (eg, target MAP of 110 mmHg or target blood
pressure of 160/90 mmHg) using intermittent or continuous
intravenous medication, and clinically reexamine the patient every 15
minutes

23. Choice of antihypertensive agent — Intravenous labetalol is
generally the first drug of choice if pharmacologic therapy is necessary
in the acute phase, since it allows rapid and safe titration to the goal
blood pressure. Other first-line agents include transdermal
nitroglycerin paste and intravenous nicardipine .
Intravenous nitroprusside should be considered second-line therapy
since it carries added theoretical risks of increasing intracranial
pressure or affecting platelet function, but in fact it is often needed.
Sublingual nifedipine should be avoided because it can cause a
prolonged and precipitous decline in blood pressure

24. Continuous infusion
rate
Intravenous bolus
dose
Drug
2 mg per minute
(maximum 300
mg/day)
5 to 20 mg every 15
minutes
Labetalol
5 to 15 mg per hourNANicardipine
25 to 300 mcg/kg per
minute
250 mcg/kg IVP
loading dose
Esmolol
NA1.25 to 5 mg IVP
every 6 hours*
Enalapril
1.5 to 5 mcg/kg per
minute
5 to 20 mg IVP every
30 min
Hydralazine
0.1 to 10 mcg/kg per
minute
NANitroprusside
20 to 400 mcg per
minute
NANitroglycerin

25. reperfusion therapy for acute ischemic
stroke
1-Intra-venous(IV) thrombolysis
2-intra-arterial (IA) thrombolysis.
3-angioplasty and stenting.
4-mechanical clot disruption.
5-combined intravenous (IV) and IA thrombolysis.
6-the combined use of fibrinolytics and GP IIb/IIIa
antagonists.

26. INTRAVENOUS THROMBOLYSIS
Results from the NINDS trial showed that intravenous
alteplase (recombinant tissue-type plasminogen activator or tPA)
improves functional outcome at three months, if given within 3 hours
of symptom onset or within 3 hours of when the patient was last seen
normal in cases when onset time is unknown
Prior to alteplase treatment, all patients require:
Confirmation that treatment is commencing within the required 4.5
hour time window after the onset of symptoms
Confirmation of a persistent, measurable neurologic deficit
Confirmation that patient selection criteria are met
Confirmation that the noncontrast head CT is without hemorrhage
Confirmation of blood pressure parameters
Two intravenous lines, preferably large bore
Accurate body weight determination

27. Eligibility criteria for the treatment of acute ischemic stroke with
recombinant tissue plasminogen activator (alteplase)
Inclusion criteria
Clinical diagnosis of ischemic stroke causing measurable neurologic
deficit with the onset of symptoms <4.5 hours before beginning
treatment; if the exact time of stroke onset is not known, it is defined as
the last time the patient was known to be normal
Exclusion criteria
Historical
Stroke or head trauma in the previous 3 months
Any history of intracranial hemorrhage
Major surgery in the previous 14 days
Gastrointestinal or urinary tract bleeding in the previous 21 days
Myocardial infarction in the previous 3 months
Arterial puncture at a noncompressible site in the previous 7 days

28. For treatment from 3 to 4.5 hours, additional relative exclusions (where
the risk/benefit ratio is less clear) are age >80 years and/or a
combination of both previous stroke and diabetes mellitus
Clinical
Spontaneously clearing stroke symptoms
Only minor and isolated neurologic signs
Seizure at the onset of stroke is an exclusion if the residual
impairments are due to postictal phenomenon; seizure is not an
exclusion if the clinician is convinced that residual impairments are
due to stroke and not to postictal phenomenon
Symptoms of stroke suggestive of subarachnoid hemorrhage
Persistent blood pressure elevation (systolic ≥185 mmHg, diastolic
≥110 mmHg)
Active bleeding or acute trauma (fracture) on examination


29. Labratory:
Platelets <100,000/mm3*
Serum glucose <50 mg/dL (<2.8 mmol/L)
International normalized ratio (INR) >1.7 if on oral anticoagulant*
For treatment from 3 to 4.5 hours, an additional relative exclusion
(where the risk/benefit ratio is less clear) is oral anticoagulant use
regardless of INR
Elevated partial thromboplastin time (aPTT) if on heparin*
Head CT scan (Evidence of hemorrhage , Evidence of a multilobar
infarction with hypodensity involving >33 percent of the cerebral
hemisphere)

30. IV alteplase administration — All patients should be
admitted to an intensive care unit or dedicated stroke unit for at
least 24 hours of close neurologic and cardiac monitoring
A dedicated intravenous line is required for alteplase, and all
patients should have at least one additional large bore
intravenous line.
The alteplase dose is calculated at 0.9 mg/kg of actual body
weight, with a maximum dose of 90 mg( Ten percent of the
dose is given as an intravenous bolus over one minute, and the
remainder infused over 1 hour)

31. Important measures during the first 24 hours of alteplase treatment
include the following:
Vital signs and neurologic status should be checked every 15 minutes
for 2 hours, then every 30 minutes for 6 hours, then every 60 minutes
until 24 hours from the start of alteplase treatment. Blood pressure
must be maintained at or below 180/105 mmHg during the first 24
hours
Anticoagulant and antithrombotic agents, such as heparin, warfarin, or
antiplatelet drugs, should NOT be administered for at least 24 hours
after the alteplase infusion is completed. Invasive procedures such
as venipuncture, catheter placement, and nasogastric tube insertion
should be avoided for at least 24 hours.
A follow-up noncontrast head CT scan should be obtained 24 hours after
alteplase is initiated if treatment with antithrombotic agents such as
aspirin or heparin is planned.

32. Management of blood pressure — Strict blood pressure control is
critical prior to and during the first 24 hours after thrombolytic therapy ,
The blood pressure must be below 185/110 mmHg prior to
administering alteplase.
Patients with blood pressure above 185/110 mmHg should be treated
with intravenous labetalol or transdermal nitroglycerin paste or
intravenous nicardipine , If this does not bring the blood pressure into
the acceptable range, the patient should not be treated with alteplase.
Once thrombolytic therapy has been administered, aggressive
measures are appropriate to control blood pressure during and for 24
hours following thrombolytic therapy , Blood pressure must be
maintained below 180/105 mmHg during this period, and liberal use of
drugs such as labetalol or sodium nitroprusside may be required.
Frequent blood pressure monitoring is recommended to ensure that
the blood pressure remains in the acceptable range and that
hypotension due to overtreatment has not occurred, which can worsen
cerebral ischemia.
Current guidelines recommend monitoring every 15 minutes for the
first 2 hours after starting thrombolytic treatment, then every 30
minutes for the next 6 hours, then every hour until 24 hours after

33. Adverse reactions to Thrombolytic ttt
1- Intracerebral hemorrhage (ICH)
should be suspected in any patient who develops sudden neurologic
deterioration, a decline in level of consciousness, new headache,
nausea and vomiting, or a sudden rise in blood pressure after
thrombolytic therapy is administered, especially within the first 24
hours of treatment. In patients with suspected ICH, the
alteplase infusion should be discontinued and a noncontrast head CT
or MRI scan should be arranged . Blood should be drawn for typing
and cross matching, and measurement of prothrombin time, activated
partial thromboplastin time, platelet count, and fibrinogen.
If ICH is confirmed by CT or MRI, the administration of agents to
reverse the effects of thrombolytic and antiplatelet therapy should be
considered, including Ten units of cryoprecipitate to increase the levels
of fibrinogen and factor VIII , Six to eight units of platelets

34. Systemic bleeding — Mild systemic bleeding usually occurs in the
form of oozing from IV catheter sites, ecchymoses (especially under
automated blood pressure cuffs), and gum bleeding; these
complications do not require cessation of treatment. More serious
bleeding, such as from the gastrointestinal or genitourinary system,
may or may not require discontinuation of alteplase depending on the
severity.
Orolingual angioedema occurs in 1 to 5 percent of patients treated
with tPA for ischemic stroke and it is typically mild, transient, and
contralateral to the ischemic hemisphere , stopping the drug infusion,
administering antihistamines and corticosteroids, and intubating
patients who develop stridor
Use in menstruating women — Thrombolytic therapy has been
found to cause an increase in moderate, but not severe, bleeding in
menstruating women

35. Intra-arterial thrombolysis
Equipment
high-resolution angiography system
catheter (Valavanis) was inserted into the femoral artery for 4-
vessel angiography
Thrombolytic agent
Urokinase (Urokinase HS Medac) in a mean dose of 863 000 IU
(range 20,000 to 1,250,000 IU)
[or alteplase 50% of standard iv dose
Technique
Inject as near as possible to or into the thrombus over 60 to 90
minutes

36. Indication:
Persistent occlusion post IV tPA < 3h
Within 6 h, but time to treatment is correlated with outcome.
IV contra-indicated
The dose of thrombolytic drugs can be limited to that needed for
recanalization, since the procedure is done under direct
visualization. The total dose of IA therapy is about one-third of the
IV dose.
In addition, mechanical disruption of the clot can be performed
and the thrombolytic drug can be infused directly into the clot.
Intra-arterial thrombolysis is an option for treatment of selected
patients who have major stroke of <6 hours’ duration due to
occlusions of the MCA and who are not otherwise candidates for
intravenous rtPA

37. -Intra-arterial thrombolysis is reasonable in patients who have
contraindications to use of intravenous thrombolysis, such as
recent surgery
-Persistent obstruction , persistent deficit
-Increase the therapeutic window
-Post-operative stroke
Advantages:
Higher concentrations delivered to the clot
Gentle mechanical disruption of the clot
Precise imaging of anatomy, pathology and collateral pattern
Exact degree and timing of recanalisation

38. combined intravenous and intra-
arterial thrombolysis
— The rationale for combined thrombolytic therapy is to
unite the advantages of each: the wide availability of
early rapid IV thrombolysis and the potentially higher
recanalization rates and therefore better outcomes of IA
thrombolysis.
.

39. Long term managment of stroke
Hypertension
— Guidelines issued in 2011 by the American Heart Association and
American Stroke Association (AHA/ASA) recommend antihypertensive
treatment for all patients with ischemic stroke and transient ischemic
attack (TIA)
The target blood pressure in this setting is not well defined, and the
AHA/ASA guidelines do not recommend a specific target
The benefit of blood pressure reduction extends to patients with and
without a history of hypertension.
The optimal antihypertensive drug regimen is uncertain but the available
data indicate that diuretics or the combination of diuretics and an ACE
inhibitor are useful.
The choice of specific drugs should be individualized with respect to
patient characteristics such as, renal impairment, cardiac disease, and
diabetes.
Lifestyle modifications that have been associated with blood pressure
reductions should be included as part of the antihypertensive regimen.
Important modifications include weight loss, salt restriction, a diet rich in
fruits, vegetables, and low-fat dairy products, regular aerobic physical
activity, and limited alcohol consumption.

40. Antithrombotic the
Recommendations
Although aspirin, clopidogrel, and the combination of extended release
dipyridamole and aspirin are all acceptable options for secondary stroke
prevention, aspirin is the only antiplatelet agent that has been established
as effective for the early treatment of acute ischemic stroke.
We recommend that early aspirin therapy (initial dose 325 mg, thereafter
150 to 325 mg/day) be given to patients with ischemic stroke who are not
receiving alteplase, intravenous heparin, or oral anticoagulants. This
recommendation is in accord with current guidelines issued by the
American College of Chest Physicians (8th edition) ,the American Heart
Association/American Stroke Association, and the National Institute for
Health and Clinical Excellence
Aspirin should not be used as an alternative to intravenous thrombolysis
or other acute therapies aimed at improving outcomes after stroke
Aspirin should be given within 48 hours of stroke onset and may also be
used in combination with subcutaneous heparin for deep vein thrombosis
prophylaxis.
The optimal dose of aspirin is uncertain; there is no compelling evidence
that any specific dose is more effective than another, and fewer side
effects occur with lower doses. Aspirin is contraindicated in patients with
aspirin allergy or active gastrointestinal bleeding. Clopidogrel or
ticlopidine are alternatives for patients intolerant to aspirin.

41. HEPARIN AND LMW — Guidelines issued in 2007 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, guidelines from the American College of Chest Physicians
(ACCP) 8th edition issued in 2008 recommend against full-dose
anticoagulation for patients with acute ischemic stroke
we suggest early anticoagulation for select patients with acute ischemic
stroke and no contraindication when stroke is due to one of the following
documented mechanisms:
-Cardioembolism from intracardiac thrombus associated with significant
valvular disease,
-severe congestive heart failure, or mechanical heart valves
-Large artery atherosclerotic stenosis with intraluminal thrombus
-Dissection of a cervical or intracranial large artery
Full-dose anticoagulation should not be used for patients with a large
infarction (based upon clinical syndrome or brain imaging findings),
uncontrolled hypertension, or other bleeding conditions

42. SMOKING national guidelines recommend smoking cessation for
patients with stroke or transient ischemic attack (TIA) and suggest
avoidance of environmental tobacco smoke

Strict glycemic control
For patients with diabetes who have had an ischemic stroke or TIA, we
suggest glucose control to near normoglycemic levels. This
recommendation is based on evidence that tight glucose control
reduces microvascular complications. However, there is no evidence
that intensive glucose-lowering therapy for patients with longstanding
type 2 diabetes reduces the risk of macrovascular outcomes such as
cardiovascular events, stroke, and death.
Diet, exercise, oral hypoglycemic drugs, and insulin are proven
methods to achieve glycemic control. A reasonable goal of therapy is
an A1C value of ≤7 percent for most patients.

43. Statin therapy: several meta-analyses have found
that treatment with statins decreases the risk of stroke in
patients with hyperlipidemia, while lipid lowering by other
means (eg, fibrates, resins, diet) has no significant impact
on stroke incidence
Obtain LDL w/in 48 h of stroke onset
◦If LDL > 100, use hi-dose statin shown to 
stroke/MI/death risk
atorvastatin 20-80 mg/d
pravastatin 40-80 mg/d
simvastatin 40-80 mg/d
rosuvastatin 10-40 mg/d
◦If LDL < 100, use lower statin dose
◦Outpatient goal LDL < 70 (but give statin to all pts)

44. Lifestyle
◦Alcohol:men < 2 oz / d, women < 1 oz / d
◦Diet:Low saturated fat, low Na+, high K+,
fruits > vegetables
◦:> 20 min aerobic exercise
◦Weight:maintain BMI 18.5-24.9 kg/m2
Drugs to Avoid
◦Estrogen (oral contraceptives, HRT)
◦Sympathomimetic agents (incl. decongestants, diet
pills)
◦NSAIDs (if taking aspirin)

45. THANK YOU