CEREBRAL VASCULAR

ACCIDENT
By: Madhava Patibanda
Vic Catania
Nazanin Zuri
Background

 Stroke is the clinical term for acute loss of perfusion to vascular

territory of the brain, resulting in ischemia and a corresponding loss of
neurologic function.

 Classified as either hemorrhagic or ischemic, strokes typically

manifest with the sudden onset of focal neurologic deficits, such as
weakness, sensory deficit, or difficulties with language.

 Ischemic strokes have a heterogeneous group of causes, including

thrombosis, embolism, and hypoperfusion

 Hemorrhagic strokes can be either intraparenchymal or subarachnoid.

Embolic strokes

 Emboli may either be of cardiac or arterial origin.

 Cardiac sources include atrial fibrillation, recent myocardial infarction,

prosthetic valves, native valvular disease, endocarditis, mural thrombi, dilated
cardiomyopathy, or patent foramen ovale allowing passage of venous
circulation emboli.

 Arterial sources are atherothrombolic or cholesterol emboli that develop in the

arch of the aorta and in the extracranial arteries (ie, carotid and vertebral
arteries).

 Embolic strokes tend to have a sudden onset, and neuroimaging may

demonstrate previous infarcts in several vascular territories or calcific emboli.
Thrombotic strokes

 Thrombotic strokes include large-vessel strokes and small-vessel or lacunar strokes. They
are due to in situ occlusions on atherosclerotic lesions in the carotid, vertebrobasilar, and
cerebral arteries, typically proximal to major branches.

 Thrombogenic factors may include injury to and loss of endothelial cells exposing the
subendothelium and platelet activation by the subendothelium, activation of the clotting
cascade, inhibition of fibrinolysis, and blood stasis.

 Thrombotic strokes are generally thought to originate on ruptured atherosclerotic plaques.

Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis.

 In other patients, especially younger patients, other causes should be considered, including
hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein S
deficiency), sickle cell disease, fibromuscular dysplasia, arterial dissections, and
vasoconstriction associated with substance abuse.
Lacunar stroke

 Lacunar strokes represent 20% of all ischemic strokes. They

occur when the penetrating branches of the middle cerebral
artery (MCA), the lenticulostriate arteries, or the penetrating
branches of the circle of Willis, vertebral artery, or basilar
artery become occluded.

 Causes of lacunar infarcts include microatheroma,

lipohyalinosis, fibrinoid necrosis secondary to hypertension or
vasculitis, hyaline arteriosclerosis, and amyloid angiopathy.

 The great majority are related to hypertension.

Watershed infarcts

 These infarcts, also known as border zone infarcts,

develop from relative hypoperfusion in the most
distal arterial territories and can produce bilateral
symptoms.

 Frequently, these occur perioperatively or in

situations of prolonged hypotension.
CT scan of right
hemispheric
ischemic stroke
CT scan showing an
intracerebral hemorrhage
with associated
intraventricular
hemorrhage.
Head CT showing deep
intracerebral hemorrhage
due to bleeding within the
cerebellum, approximately
30 hours old.
Causes

 Risk factors for ischemic stroke comprise both

modifiable and nonmodifiable etiologies.

 Identification of risk factors in each patient can

uncover clues to the cause of the stroke and the
most appropriate treatment and secondary
prevention plan.
 Nonmodifiable risk factors include age, race, sex,
ethnicity, history of migraine headaches, sickle cell
disease, fibromuscular dysplasia, and heredity.
 Modifiable risk factors include the following:
 Hypertension (the most important)
 Diabetes mellitus
 Cardiac disease - Atrial fibrillation, valvular disease, mitral stenosis, and
structural anomalies allowing right to left shunting, such as a patent
foramen ovale and atrial and ventricular enlargement
 Hypercholesterolemia
 Transient ischemic attacks (TIAs)
 Carotid stenosis
 Hyperhomocystinemia
 Lifestyle issues - Excessive alcohol intake, tobacco use, illicit drug use,
obesity, physical inactivity
 Oral contraceptive use
History

The American Stroke Association advises the public to be aware

of the symptoms of stroke that are easily recognized and to call
911 immediately. These symptoms include the following:

 Sudden numbness or weakness of face, arm, or leg, especially on

one side of the body
 Sudden confusion, difficulty in speaking or understanding
 Sudden deterioration of vision of one or both eyes
 Sudden difficulty in walking, dizziness, and loss of balance or
coordination
 Sudden, severe headache with no known cause
 A focused medical history aims to identify risk
factors for atherosclerotic and cardiac disease,
including hypertension, diabetes mellitus, tobacco
use, high cholesterol, and a history of coronary artery
disease, coronary artery bypass, or atrial fibrillation.

 Consider stroke in any patient presenting with acute

neurological deficit or any alteration in level of
consciousness.
 Common signs of stroke include the following:

 Acute hemiparesis or hemiplegia

 Complete or partial hemianopia, monocular or
binocular visual loss, or diplopia
 Dysarthria or aphasia
 Ataxia, vertigo, or nystagmus
 Sudden decrease in consciousness
 A thorough history can be vital in assessment:
 For younger patients: h/o recent trauma, coagulopathies,
illicit drug use (especially cocaine), migraines, or use of
OCP
 People around the pt at the time of incident can be useful in
information regarding the time and events surrounding the
onset of symptoms
 Thisis needed as establishing the time the patient was last
normal is especially critical for thrombolytic Tx
 If the patient awakens with the symptoms, then the time of onset is
defined as the time the patient was last seen without symptoms
Physical Examination
 The physical examination can be considered to be
subdivided or focused toward 5 areas:
 Assessing airway, breathing, and circulation (ABCs)
 Defining the severity of neurological deficit
 Etiology
 R/o CVA mimics
 Identification of associated Sx/comorbidities
 While the exam can be thought of subdivisions, it is
vital that all major organ systems be kept in mind
and quickly assessed
 This ties directly to the types of CVA a pt may present
with:
 Hemorrhagic pts will deteriorate rapidly and require
intervention, while those with an ischemic insult tend to not
have ABC problems
 Do not underestimate vital signs as they can be a quick
indicator if a pt is on the decline
Vitals
 Many patients with stroke are hypertensive at
baseline, and their blood pressure may become
more elevated after stroke.
 While HTN at presentation is common, BP may
decrease spontaneously over time in most patients.
 This is relevant as acutely lowering blood pressure has
not proven to be beneficial in CVA pts in the absence
of signs and symptoms of associated malignant HTN,
AMI, CHF, or aortic dissection.
 HEENT: Contusions, lacerations, and deformities may suggest
trauma; auscultation of the neck may elicit a bruit suggesting carotid
disease as the cause of the stroke.

 CVS: Cardiac arrhythmias, such as atrial fibrillation, are found

commonly in patients. CVA may also occur with other AMI and acute
CHF exacerbation necessitating auscultation for murmurs and gallops.

 Extremities: Carotid, vertebrobasilar, and occasional thoracic aortic

dissections may cause ischemic stroke.
 Unequal pulses or blood pressures in the extremities may reflect the
presence of aortic dissections.
 A key quantifier from a neurological standpoint is the
National Institutes of Health Stroke Scale (NIHSS).
 This scale provides insight to the location of vascular lesions
and is correlated with outcome in patients with ischemic
stroke.
 It focuses on 6 major areas of the neurologic
examination:
 level of consciousness
 visual function
 motor function
 sensation and neglect
 cerebellar function
 The NIHSS enables the rapid determination of the
severity and possible location of the stroke.
 A patient's score on the NIHSS is strongly
associated with outcome, and it can help identify
those patients who:
 are likely to benefit from thrombolytic therapy
 those who are at higher risk to develop hemorrhagic
complications of thrombolytic use
Differential Diagnosis
• Bell Palsy  Hyperglycemia
• Meningitis  Hypoglycemia
• Brain Abscess  HTN urgency
• Migraine Variants  HTN emergency
• Brain Metastasis  Ingestions (e.g., ethanol)
• Seizures/Epilepsy  Spinal injury
• Cerebral Venous Thrombosis  Uremia
• Subdural Hematoma
 Conversion Disorders
• Transient Global Amnesia
•
 Viral Encephalitis
Epidural Hematoma
 Dizziness/Vertigo/balance
Labs
 Glucose level
 BMP/CMP
 CBC: important in fibrinolytic candidates
 PT and aPTT tests: Tx decisions require data on coagulation status
 INR
 Cardiac enzymes: used to r/o concomitant AMI
 ABG: defines the severity of hypoxemia; if considering thrombolytics avoided unless
absolutely necessary
 Additional laboratory tests:
 Toxicology screen
 Fasting lipid profile
 ESR
 Pregnancy test
 ANA
 In select patients with possible hypercoagulable states, protein C, protein S, antithrombin III, and
Factor V Leiden testing may be required
Imaging
 CT w/o contrast: very sensitive in detecting intracerebral and subarachnoid hemorrhage, as well
as subdural hematomas
 Loss of the gray-white matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of
early ischemia
 A dense MCA sign suggests a clot in the MCA, potentially producing large hemispheric strokes.
 CT may demonstrate other causes of the patient's symptoms, including neoplasm, hemorrhagic stroke,
epidural and subdural hemorrhage, aneurysm, abscess, arteriovenous malformation, and hydrocephalus
 CT angiography may demonstrate the location of vascular occlusion
 MRI with magnetic resonance angiography (MRA): can demonstrate impaired metabolism
 Digital subtraction angiography: definitive method for demonstrating vascular lesions, occlusions,
stenoses, dissections, and aneurysms.
 Cerebrovascular angiography not only provides useful information on vasculature, but also allows for
intra-arterial therapies
 Carotid duplex
 Transcranial Doppler ultrasonography (TCD): assess the location and degree of arterial
occlusions in the extracranial carotid and large intracranial vessels
 used to detect restoration of flow after thrombolytic therapy
Other Procedures
 Echo: Transthoracic echocardiography (TTE) and
transesophageal echocardiography (TEE) are useful tools
in evaluating patients with possible cardiogenic sources of
their stroke
 EKG: Stroke and cardiovascular disease share many risk
factors
 Chest radiography should be performed when clinically
indicated
 LP: R/o meningitis or subarachnoid hemorrhage when the
CT scan is negative but the clinical suspicion remains high
 Stroke Treatment

Stabilization


Stabilization may need to precede



complete evaluation.
 Comatose or obtunded patients (eg,
Glasgow Coma Score ≤ 8)
may require airway support such as
mechanical ventilation.
 Increased intracranial pressure is

suspected
 intracranial pressure monitoring and
measures to reduce cerebral edema
 Stroke Treatment
 Intracerebral Hemorrhage
 Supportive measures and control
of general medical risk factors.
 Anticoagulants and antiplatelet
drugs are contraindicated.
 If patients have used anticoagulants,
the effects are reversed
 fresh frozen plasma,
 vitamin K
 platelet transfusions
Stroke Treatment
 Intracerebral Hemorrhage
 Hypertension
Treated only if mean arterial pressure is > 130 mm
Hg or systolic BP is > 185 mm Hg.
Nicardipine 2.5 mg/h IV is given initially; dose is
increased by 2.5 mg/h q 5 min to a maximum of 15
mg/h as needed to decrease systolic BP by 10 to 15%.
 Cerebellar hemisphere hematomas that are > 3 cm in
diameter may cause midline shift or herniation
surgical evacuation is often lifesaving.
 For large lobar cerebral hematomas
early surgical evacuation may be lifesaving
 rebleeding occurs frequently,

 sometimes increasing neurologic deficits.

 For deep cerebral hematomas

early surgical evacuation is seldom indicated
surgical mortality is high and neurologic deficits are
usually severe.
 Stroke Treatment
 Ischemic Stroke
 Perfusion of an ischemic brain area may
require a high BP because autoregulation
is lost
 BP should not be decreased except in the
following situations:
 BP is > 220 mm Hg systolic or > 120 mm
Hg diastolic on 2 successive readings > 15
min apart.
 There are signs of other end-organ damage
(eg, aortic dissection, acute MI, pulmonary
edema, hypertensive encephalopathy, retinal
hemorrhages, acute renal failure).
 Use of recombinant tissue plasminogen
activator (tPA) is likely.
 Nicardipine or IV Labetalol can be used to
lower BP
 Stroke Treatment
 Ischemic Strokes
 Patients with presumed thrombi or emboli may be treated with tPA,
thrombolysis-in-situ, antiplatelet drugs, and/or anticoagulants.
 Recombinant tPA must be given within 3 h of symptom onset.
 Because the precise time of symptom onset may not be known, clinicians must start
timing from the moment the patient was last observed to be well.
 Before treatment
 Brain hemorrhage must be excluded by CT
 Systolic BP must be <185 mm Hg and diastolic BP <110 mm Hg
 antihypertensive drugs may be given
 Dose of tPA is 0.9 mg/kg IV (maximum dose 90 mg)
 10% is given by rapid IV injection, and the remainder by constant infusion over 60
min.
 Vital signs are closely monitored for 24 h after treatment,
 BP is maintained below the target levels listed above.
 Any bleeding complications are aggressively managed.
 Anticoagulants and antiplatelet drugs are not used within 24 h of treatment with
tPA.
 Stroke Treatment
 Ischemic Stroke
 Most patients are not candidates
for thrombolytic therapy; they
should be given an antiplatelet
drug

 Contraindications to antiplatelet
drugs include aspirin- or
NSAID-induced asthma or
urticaria, other hypersensitivity
to aspirin, acute GI bleeding,
G6PD deficiency.
 Stroke Treatment
 Oral antiplatelet drugs used
 Aspirin 81 or 325 mg once/day
 Clopidogrel 75 mg once/day
 In patients taking warfarin, antiplatelet
drugs additively increase risk of
bleeding and are thus usually avoided;
however, aspirin is occasionally used
simultaneously with warfarin in certain
high-risk patients.
 The combination of clopidogrel and
aspirin is avoided because it has no
advantage over aspirin alone and
results in more bleeding complications.
 Stroke Treatment
 Ischemic Stroke
 Heparin or low molcular weight heparin
 for stroke caused by cerebral venous
thrombosis
 for emboli due to atrial fibrillation
 Warfarin is begun simultaneously with
heparin .
 Before anticoagulation, hemorrhage must
be excluded by CT.
 PTT should be 1.5 to 2 times baseline
values until warfarin has increased the
INR to 2 to 3
Stroke Treatment
 Ischemic Strokes
 Thrombolysis-in-situ
(angiographically directed intra-
arterial thrombolysis) of a
thrombus or embolus
 sometimes be used for major
strokes if symptoms have begun >
3 h but < 6 h ago
 Specially for strokes due to large
occlusions in the middle cerebral
artery.
 Clots in the basilar artery may be
intra-arterially lysed up to 12 h
after stroke onset.
 Stroke Treatment
 Transient Ischemic Attacks
 initial treatment is aspirin
 second line is clopidogrel
 third line is ticlopidine
 If TIA is recurrent after aspirin
treatment, the combination of aspirin
and dipyridamole is needed (Aggrenox).
 Carotid endarterectomy or arterial
angioplasty plus stenting can be useful
for some patients, particularly those who
have no neurologic deficits but who are
at high risk of stroke.
Stroke Treatment
 Subarachnoid Hemorrhage
 Hypertension
 Nicardipine if mean arterial pressure is > 130 mm
Hg
 BP needs to be maintained between mean arterial
pressure of 70 to 130 mm Hg and a systolic pressure
of 120 to 185 mm Hg
 Vasospasm
 prevented by giving Nimodipine 60 mg po q 4 h for
21 days
 Stool softeners are given to prevent constipation,
which can lead to straining.
 Anticoagulants and antiplatelet drugs are
contraindicated.
Stroke Treatment
 Subarachnoid Hemorrhage
 Aneurysms
 occluded to reduce risk of rebleeding.
 Detachable endovascular coils can be inserted
during angiography to occlude the aneurysm.
 if the aneurysm is accessible, surgery to clip
the aneurysm or bypass its blood flow can be
done
 If patients are arousable operation is within
the first 24 h to minimize risk of rebleeding.
 If > 24 h have elapsed, delay surgery until 10
days have passed
Prevent and Treat Stroke Complications
 Strategies to Prevent and Treat Stroke Complications
 Applying tight elastic or air-filled support stockings and providing frequent
active and passive leg exercises
 Turning bedridden patients frequently, with special attention to pressure sites
 Passively moving limbs at risk of contractures and placing them in the
appropriate resting positions, using splints if necessary
 Ensuring adequate fluid intake and nutrition, including evaluating patients for
swallowing difficulties and providing nutritional support as necessary
 Giving small doses of heparin (5000 U) sc q 12 h or an equivalent amount of
low mol wt heparin (LMWH) to prevent deep venous thrombosis and
pulmonary embolism
 Encouraging early ambulation (as soon as vital signs are normal), with close
monitoring
 Maximizing lung function (eg, smoking cessation, deep breathing exercises,
respiratory therapy, measures to prevent aspiration in patients with dysphagia)
Prevent and Treat Stroke Complications

 Looking for and treating infections early, especially pneumonia, UTIs,

and skin infections
 Managing urinary bladder problems in bedridden patients, preferably

without using an indwelling catheter

 Promoting risk factor modification (eg, smoking cessation, weight loss,

healthful diet)
 Prescribing early rehabilitation (eg, active and passive exercises, range-

of-motion exercises)
 Compassionately discussing residual function, prognosis for recovery,

and strategies to compensate for lost function with the patient

 Encouraging maximum independence through rehabilitation

 Encouraging the patient and family members to contact stroke support

groups for social and psychologic support

Question 1
Signs and symptoms of a stroke include facial
droop, aphasia, and:

A. Bilateral equality of function.

B. Pronater drift.
C. Eyes "locked" in the lateral position.
D. Left arm or jaw pain.  
Question 2
Hemorrhagic strokes often occur in people:

A. Taking blood-thinning medication.

B. While they are asleep.
C. With a history of heart attack.
D. With a history of high blood pressure.