Transcript Ischemic Stroke

Strokes in the Elderly
Edward Via Virginia College of Osteopathic Medicine
Donald Noll DO FACOI
Edited by
Dr. Edward Warren
Chair, Geriatrics
Carolinas Campus
May 2012
GOAL
To understand the signs and symptoms of
stroke, its proper evaluation, and its
management.
Learning Objectives
1.
2.
3.
4.
5.
6.
7.
8.
Define stroke. (slide 5)
List and describe the kinds of stroke.
(slides 6 – 13)
List the risk factors of stroke. (slide 14)
Describe the symptoms of stroke. (slide 15)
List and describe the territorial stroke syndromes. (slides 16 – 24)
Discuss the history taking in a stroke victim. (slides 25 – 26)
Discuss the physical in a stroke victim.
(slides 27 – 28)
Assess and describe baseline and current functional abilities
(instrumental activities of daily living, activities of daily living, and
special senses) in an older patient by collecting historical data from
multiple sources and performing a confirmatory physical
examination. (slides 29 – 32)
Learning Objectives
9.
10.
11.
12.
13.
List the differential diagnosis of stroke. (slide 33)
List laboratory testing useful in stroke.
(slides 34 – 35)
Discuss imaging studies useful in stroke.
(slides 36 – 42)
Describe treatment of stroke. (slides 43 – 47)
Develop a preliminary management plan for patients presenting
with functional deficits, including adaptive interventions and
involvement of interdisciplinary team members from appropriate
disciplines, such as social work, nursing, rehabilitation, nutrition,
and pharmacy. (slide 48)
14. Discuss prevention of stroke. (slide 49)
General Considerations
• Stroke is a neurologic deficit with a vascular etiology
lasting over 24 hours.
• Cerebral Vascular Accident is a synonym for stroke.
• Stroke is third leading cause of death in the United States.
• Cerebral ischemia is a reduction of blood flow and oxygen to
the brain resulting in prompt neurologic deficits. If it persists,
then infarctions of brain tissue occur with ischemic
encephalopathy.
• Transient ischemic attacks (TIA’s) are ischemia induced
neurologic deficits persisting for < 24 hours. They generally
resolve shortly.
Types of Stoke
• Ischemic strokes occur from occluded arteries to part or all of the
brain, resulting in brain infarction.
• This is the most common type of stroke (80%)
• It can be thrombotic where a clot forms in the artery
• It can be embolic where clots break away upstream and lodge in the
artery distally.
• Hemorrhagic Strokes occur from bleeding inside or around the brain
(20%)
• Must be ruled out first, since treatment is vastly different.
• Blood caused tissue swelling and edema, producing a “mass effect” in
the brain.
Pathogenesis of Stroke
•
•
•
•
Atherosclerosis is the most common cause of stroke
Plaques cause strokes in three ways:
•
Thrombosis forms at the site of an atherosclerotic lesion, and the clot
obstructs the artery there;
•
Ulceration or rupture of a plaque leads to formation of a clot with emboli to
distal sites
•
Hemorrhage into a plaque obstructs the artery.
The clinical manifestations of a stroke depend on the rate of occlusion. If it occurs
slowly, there may be time for collaterals to develop, and a stroke is avoided.
If the occlusion is abrupt, a stroke ensues. The degree of damage depends on the
collaterals available to the territory of the brain that is supplied by the occluded
vessel.
Hemorrhagic verses Ischemic
•
•
Early on, when acute therapy is
potentially beneficial, it is
impossible to predict whether a
patient will recover
spontaneously.
Hemorrhagic strokes are promptly
diagnosed by seeing extravasated
blood in the brain parenchyma,
usually on a STAT CT scan.
• Ischemic strokes can later bleed
into the necrotic tissue,
converting to hemorrhagic ones.
Lacunar Infarction
• Small ischemic strokes, usually < 5 mm in size
• Localized in the basal ganglia, pons, cerebellum, anterior limb
of the internal capsule, and the deep cerebral white matter
• Associated with poorly controlled HTN and DM
• Cause pure contralateral motor or sensory loss, ipsilateral ataxia,
dysarthria, or ataxia
• Sometimes visible on CT scan as a punched out lesion, hypodense,
but often unseen
• Relatively good prognosis, partial or complete resolution common
in 4 to 6 weeks
Emboli
• Pieces of larger clots that
break off from a mural
thrombus in the heart or a
more proximal artery and
lodge downstream in the
brain distally.
• It is often impossible to
distinguish thrombus from
embolus by imaging
methods, so the two
processes are classified
together.
Hemorrhagic stroke
• Often severe at onset and
may present with
headache and rapidly
evolving deficits
• Ischemic strokes are
normally painless and
present as a fixed deficit or
with a stuttering onset
followed by rapid waxing
and waning fluctuations
Subarachnoid Hemorrhage
• It presents as a sudden and very severe headache (the worst
headache of my life). Signs of meningeal irritation are usually
present. Symptoms of mental confusion and obtundation are common.
Focal deficits are frequently absent.
• The CT scan is the best test to detect this promptly. Blood in the
cerebrospinal fluid confirms subarachnoid hemorrhage, even if the CT
scan is negative.
• Treat with supportive care, slowly lower elevated blood pressure, but not
below a diastolic level of 100mm Hg. Many patients are treated with
phenytoin to prevent seizures prophylactically.
CEREBRAL VENOUS SINUS THROMBOSIS
• Presents as headache, focal neurologic deficits, seizures, altered
mental status, and papilledema.
• Obstruction of the superior sagittal sinus is very serious andoften involves
the veins draining the superior and medial surfaces of both cerebral
convexities.
• This results in bilateral weakness and sensory changes in the legs.
• Seizures occur more often with venous than with arterial occlusion.
• These venous occlusions occur most commonly in association with
coagulopathies, often in the puerperal period, or in patients with
disseminated cancer. The transverse sinus can be occluded as a
consequence of inner ear infections, a condition called otitic
hydrocephalus.
Major Risk Factors for Stoke
•
•
•
•
•
•
•
•
•
•
hypertension
diabetes mellitus
hyperlipidemia
cigarette smoking
cardiac disease
AIDS
recreational drug use
heavy alcohol consumption
family `history of a stoke
personal history of stroke
SYMPTOMS OF STROKE
 At first neurologic symptoms and signs fluctuate and
then deteriorate rapidly.
 Many patients delay seeking medical care due to denial
hoping for improvement. Often, it is family and friends
who bring stroke patient to the ER or doctor’s office.
Prompt attention is crucial for intervention to work.
 If the symptoms completely resolve in 1 or 2 hours, the
patient had a TIA. This resolution is from dissolution of
the embolus with restoration of normal regional blood
flow and decreased vasospasm.
Vascular Territory & Stroke Syndromes
The next 8 slides define the patterns of
paralysis and neurologic dysfunction see in
different parts of the brain and different parts
of the cerebral vasculature are affected.
INTERNAL CAROTID ARTERY
• The common carotid artery bifurcation is the most
common site for atherosclerotic lesions of the cerebral
vessels.
• Occlusion of the internal carotid artery (ICA) is often
clinically silent if the circle of Willis is complete
• It is often impossible to distinguish ICA occlusion from
similar damage to the middle cerebral artery (MCA) on
clinical examination. Because the ophthalmic artery
originates from the ICA, however, TIAs of the ICA may
present as transient monocular blindness (called amaurosis
fugax)
ANTERIOR CEREBRAL ARTERY
• Isolated occlusion of the anterior cerebral artery (ACA) is only 2%
of all cerebral infarcts.
• The principal symptoms associated with occlusion of an ACA are upper
motor neuron weakness and cortical sensory signs deficits (neglect) in the
contralateral leg.
• Other manifestations of ACA occlusion may include:
– Urinary incontinence,
– Generalized depression of psychomotor activity (abulia),
– Aphasia with loss of verbal fluency, but preserved ability to repeat.
– Bilateral occlusion may occur because the origins of the two ACAs are
close together. They are occasionally from a common source
– Bilateral damage usually causes a patient to be mute, with severe mood
disturbances, and long-lasting incontinence from the damaged frontal
lobes.
MIDDLE CEREBRAL ARTERY
• Strokes involving the MCA are the most common type of focal
ischemic stroke, causing approximately two thirds of all infarcts.
• Occlusion of the stem of the MCA causes massive, devastating
infarction of the hemisphere.
• Cerebral edema during the first 3 to 4 days may lead to increased
intracranial pressure with brain herniation.
• The classic picture of occlusion of the MCA is contralateral weakness
and sensory loss in the face and arm (with relative sparing of the leg)
and homonymous hemianopia on the side of the weakness.
• Gaze deviates toward the side of the lesion.
• Full recovery is unlikely. In right-handed people, occlusion of the left
MCA produces global aphasia which is both receptive and expressive.
• In the nondominant hemisphere, unilateral neglect, anosognosia
(unawareness of the deficit), and spatial disorientation occur.
Embolus to the MCA
• Often lodges in one of its two main divisions
• Occlusion of the superior division can cause dense
sensorimotor deficits in the contralateral face and arm
without initial impairment of alertness
• Occlusion of the inferior division in the dominant
hemisphere characteristically produce receptive aphasia of
Wernicke's type (severe loss of speech comprehension with
preserved spoken and written language)
• Damage to either hemisphere can cause contralateral loss of
integrated sensation, such as perception of shapes
(stereognosis)
POSTERIOR CEREBRAL ARTERY
•
•
•
•
•
Both posterior cerebral arteries (PCAs) arise from the basilar artery ¾
of the time.
One PCA can arise from the basilar artery, and the other from the ICA, or
both from the ICA’s. Thus, the syndromes associated with occlusion of the PCA
are variable.
Strokes of the perforating branches cause complete contralateral hemianesthesia
with loss of all sensation and complete ipsilateral hemianopsia.
Macular (central) vision may be spared because of collateral blood supply from
the MCA. Difficulty reading (dyslexia) and performing calculations (dyscalculia)
may occur. Recovery is often good, but the initial numbness may be replaced by
paresthesias or excruciating pain: Dejerine-Roussy syndrome from damage to
the thalamus.
Involvement of the subthalamic nucleus may produce hemiballismus, with wild
flinging movements of the limbs on one side of the body
VERTEBRAL AND BASILAR ARTERIES
• Occlusion of the blood supply to the brain stem causes a crossed syndrome with a
contralateral weakness and selected contralateral and ipsilateral sensory symptoms
below the level of the lesion, plus ipsilateral motor and sensory deficits localizing to
the level of the lesion.
• Weber's syndrome is a mesencephalic hematoma that produces an ipsilateral third cranial nerve
palsy, resulting from damage to the oculomotor nucleus, plus contralateral weakness.
• The vertebral arteries are the principal blood supply for the medulla. The posterior inferior
cerebellar artery is usually a branch of the vertebral artery. The consequences of occlusion of a
posterior inferior cerebellar artery vary.
• Lateral medullary infarction with Wallenberg's syndrome is classically produced. In about 80%
of cases, an occlusion of the vertebral artery causes lateral medullary syndrome, which consists
of severe vertigo, nausea, vomiting, nystagmus, ipsilateral ataxia (of the cerebellar type), and
ipsilateral Horner's syndrome (ptosis, myosis, and decreased sweating).
• This syndrome also includes an ipsilateral loss of facial pain and temperature sensation and a
contralateral loss of these in the trunk and limb.
Basilar Artery
Supplies most of the brain stem.
Its occlusion produces a variety of syndromes.
Obstruction of the trunk is often fatal.
Coma may occur, or patients may develop the
locked-in syndrome, in which consciousness is
preserved, but the victims are unable to move
anything voluntarily except for their eyes or
eyelids.
• It is possible to communicate with these patients
and demonstrate normal mental status by codes
involving eye movements.
•
•
•
•
Brain Stem Strokes
• Although small, ischemic
strokes in the brain stem
can produce major
neurologic dysfunction
• Tey may not be detected
by CT
• Brainstem hemorrhage
also possible
HISTORY: Key things
• As always, get the compete story of the HPI: onset, duration,
symptoms, severity, modifying factors, etc. This is often neglected
and is the most important evaluation to make the correct diagnosis.
• Note if the onset on symptoms was less than three hours ago. If it
was an ischemic stroke, and the patient is a candidate, thrombolytic
therapy can be done.
• Get a good past medical history, covering risk factors for stroke and
any history of previous stroke.
History
• TIA’s usually resolve quickly, certainly within
the first hour or two
• Rapid progression of deficits or the presence of
headache occurs more often in patients with
intracerebral hemorrhage
• There is some diurnal variation in the onset of
stroke, with a peak in the late morning.
PHYSICAL EXAMINATION
• The neurologic exam is cost-effective and localizes the site of the lesion
• The cardiovascular examination
– arterial blood pressure (both arms); consider aortic dissection or subclavian
steal
– Extremely elevated blood pressure can lead to heart failure that may have to be
managed urgently.
– Overly aggressive reduction of BP may cause hypotension and enlarge the infarct.
– The pulse may reveal arrhythmias, such as atrial fibrillation, that can cause
cerebral embolism.
– Cardiac murmurs may suggest valvular lesions that can cause cerebral embolism
– Bruits of the carotid arteries can be produced by atherosclerotic disease of the
arteries that is associated with embolic and thrombotic strokes.
– Evidence of peripheral vascular disease may be a reflection of generalized
atherosclerosis.
Neurologic Exam
• If the patient's mental status is depressed, bilateral cerebral
lesions or a brain stem lesion is suggested.
• Multiple smaller strokes may lead to dementia.
• Speech is commonly affected, with various aphasic patterns
suggesting the site of the lesion.
• The testing of strength, sensation, and deep tendon reflexes
provides information about the patterns of the deficits and
suggests the site of the vascular lesion.
• Plantar stimulation (Babinski's sign), which is a classic finding in
damage to long tracts, indicates upper motor neuron damage
caused by strokes
• During the early phases of a large stroke, reflexes may be
depressed rather than hyperactive.
Special Senses
• Vision: check whether they can see to only
one side (a homonymous hemianopsia), or
not at all. Ask to count fingers. Notice if they
look only to one side.
• Hearing: this is obvious when you begin to
speak with them.
• Taste and smell can be tested if you are
equipped with proper testing materials:
perfume, salt, sugar, vinegar
Functional Assessment
• Activities of Daily Living (ADL’s)
– There are 4 for the lumpers: mobility, dressing, feeding,
and toileting
– There are 6 for the splitters who divide toileting into
bathing, grooming, and body waste elimination
• Instrumental ADL’s (IADL’s)
– There are 7 of these more complex tasks required for full
self care.
• Assess all of these in the history and physical by
examination and questioning of the patient and family.
ADL’s
• Functional Mobility: walking with or without aids, transferring
and moving about with a wheelchair
• Dressing: selecting clothes and putting them on
• Feeding: feeding oneself food and beverages
• Toiletting: everything one does in a bathroom
– Bathing: cleaning oneself at a sink, in a bath, or in a shower (with or
without a chair)
– Grooming: shaving, combing, brushing teeth, flossing brushing hair,
applying deodorant
– Going to the toilet: elimination of urine and stool with appropriate
cleansing as required
IADL’s
1.
2.
3.
4.
5.
6.
7.
Housework: cleaning, maintenance, vacuuming, sweeping,
dusting, bed making, laundry
Meal preparation: Preparing adequate meals for oneself
Taking medications: Accurately giving oneself one’s own medicines
Managing money: Paying bills and keeping track of banking
matters (?balancing checkbook?)
Shopping: for food, clothing, and other household needs
Telephoning: communicating effectively for social interaction and
providing for one’s needs (emergencies, computer use)
Handling transportation: public or private to get places (stores,
physician offices, appointments, social engagements)
Differential Diagnosis
• Seizure: Following a seizure, is a postictal period of mental fogginess
during which temporary neurologic deficits may manifest. This is called
Todd’s Paralysis. It is differentiated from a stroke by the history of seizures.
• Tumor: Brain tumors may present as acute focal neurologic deficits. Tumors can
cause cerebral bleeding, seizures, hydrocephalus, and a mass effect from cerebral
edema. Imaging studies will usually identify a tumor.
• Migraine Headaches: These can present with symptoms of cerebral ischemia
and focal deficits at the onset. The pain classically occurs afterward, but some
have no pain making diagnosis difficult.
• Metabolic Encephalopathy: Neurologic damage from prior strokes can become
“unmasked” during periods of metabolic encephalopathy from fever, infection,
hypoglycemia, hypercalcemia, or hepatic encephalopathy. The deficits resolve
when the condition is treated.
LABORATORY EXAMINATION
CBC
• Polycythemia leads to hyerviscosity resulting in stroke
• Thrombocytosis leading to hypercoagulable states
• High WBC from bacterial endocarditis showering the brain with septic emboli
• Severe anemia with poor oxygen carrying capacity
Erythrocyte Sedimentation Rate
• Elevated in patients with hypercoagulable states
• Markedly elevated in patients with polymyalgia rheumatica and associated giant
cell arteritis
Blood glucose level
• Hyperglycemia and hypoglycemia can produce focal and global neurologic
deficits
• Diabetes increases the risk of a stroke
LABORATORY EXAMINATION
PT and INR
• Determines whether warfarin patients have been taking their
medications or are excessively anticoagulated.
EKG
• Atrial fibrillation which causes embolic strokes
• Acute myocardial infarctions
• Echocardiogram to detect valvular lesions and vegetations if
clinically indicated.
Spinal tap
• Detects subarachnoid hemorrhage and helps provide its age
• Neurosyphilis is diagnosed with a positive CSF VDRL.
• Meningitis
Imaging
• A STAT CT scan of the head without contrast is obtained first to rule
out hemorrhage.
• CT scanning is superior to an MRI scan for detecting intracranial
hemorrhage in the first 48 hours of a bleed and it is quicker to do.
• The initial CT scan may not detect cerebral ischemia or differentiate a
tumor from cerebral ischemia, which is why a 2nd CT or MRI scan is
ordered after 24 - 48 hours to reveal the ischemic stroke region.
• Cerebral angiography or MRI angiography are ordered to determine the
source of bleeding, identify aneurysms, and AV malformations in
hemorrhagic strokes.
CT scan imaging studies
Ischemic Infarction
• Subtle infarct has only
scattered red cells
• Noted to the right:
recent ischemic
infarct due to
thrombosis of the left
middle cerebral artery
(less than 12 hours)
Hemorrhagic Conversion
• Varies from patchy
petechial bleeding
to confluent
hemorrhage
• In general do not
fully anti-coagulate
a brain infarct
MRI
• More sensitive than CT
for detecting early
ischemia, but not blood
• MRI cannot be used in
patients who have
ferromagnetic materials
within their bodies
MRI Image
An infarction, visible on an
MRI, indicates a patient has
had a small subcortical
stroke. Multiple infarctions
indicate the patient has had
numerous subcortical strokes
that could lead to severe
disability and cognitive
decline (dementia) in this
patient.
CEREBRAL ANGIOGRAPHY
• Reserved for
patients who are
suspected to have a
surgically
correctable lesion
• Arterial vessels are
displayed initially,
and delayed images
can outline the
venous system
This is a brain magnetic resonance angiogram (MRA).
The image is a "scout" image of the Circle of Willis at the
base of the brain. The yellow arrows point to 6 different
brain aneurysms.
Ischemic Stroke: treatment
• Anticoagulate with heparin to limit the size of the stroke.
• Cerebral edema is managed with prednisone or
dexamethasone.
• Treatment is mainly supportive. Correct dehydration.
• Blood pressure should be lowered with caution, since cerebral
autoregulation of blood flow is disturbed and lowering it too
rapidly can extend the stoke. Lower blood pressure cautiously
to a systolic 170 - 200 & diastolic of 100 for the first two weeks
following an ischemic stroke.
• Anti-coagulation for patient with an embolic source is crucial.
Titrate warfarin to an INR of 2.0 to 3.0
Ischemic Stroke: Treatment
 Physical therapy, occupational therapy and speech therapy to
restore function.
 Prognosis for an ischemic stroke is better than that for a cerebral
bleed or subarachnoid hemorrhage.
 The larger the infarction the worse the prognosis.
 One stroke increases the chances of suffering another stroke.
 Lowering serum cholesterol and other risk factors, lowers the risk
of future ischemic strokes.
 Anti-platelet therapy reduces the risk of a future ischemic stroke
by about 30%.
 In one two year comparison study, warfarin was not shown to be
proven to be superior to aspirin in ischemic stroke.
Thrombolytic Therapy
• Thrombolytic therapy is for acute management of
ischemic stroke if given within 3 hours of onset.
• Intravenous:
– tissue plasminogen activator (tPA),
– streptokinase, or
– intra-arterial recombinant prourokinase (rpro-UK).
• Thrombolytic therapy can improve the chances for a full or
nearly full clinical recover by about 30%.
• Most ER’s have protocols written up to follow.
TPA FOR ACUTE ISCHEMIC STROKE
Clinical presentation—focal neurologic deficits
Patient selection
Therapy must be started within 3 hr of acute ischemic stroke symptom onset
A baseline CT scan must be obtained before therapy initiation
Contraindications
Evidence of intracranial hemorrhage on pretreatment evaluation
Suspicion of subarachnoid hemorrhage
Recent intracranial surgery, serious head trauma, or previous stroke
History of intracranial hemorrhage
Uncontrolled hypertension at time of treatment - >185 systolic or >110 diastolic - that cannot be reduced with acute therapy
Seizure at stroke onset
Active internal bleeding
Intracranial neoplasm, AVM, or aneurysm
Known bleeding diathesis, including but not limited to:
Oral anticoagulation with prothrombin time >15 sec
Heparin administration within preceding 48 hr and elevated activated partial thromboplastin time at presentation
3
Platelet count <100,000/mm
Acute Stroke Thrombolysis
In this angiogram, an
artery in the brain (left
middle cerebral) is
blocked. When clot
dissolving medicine is
injected directly into
the artery, combined
with mechanical clot
disruption, blood flow
is restored.
Management Plan
•
•
•
•
•
•
Involve the entire interdisciplinary team in rehab to share the load
and to be more effective yourself.
Social workers will help with disposition and resources in the community.
Nursing will carry the load of daily care and deserves your respect and
support. They can also advise you how to treat many aspects of daily care
needs.
Rehabilitation will help provide therapy to deal with weakness, debility, and
dysfunction.
Dietary may have advice about nutritional options, especially for those who
are limited in ability to take nourishment or who are fed artificially and
having digestive symptoms.
Pharmacy can advise you about the likelihood of interactions and timing of
medications. A complicated regimen is a daunting task. The cytochrome
P450 and P-gP interactions alone will be better handled as a team.
Prevention of Stroke
• Hypertension is the most important risk factor for ischemic
and hemorrhagic stroke
• Approximately 10% of men and 7% of women older than age 65
have asymptomatic carotid stenosis over 50% occluded.
Epidemiologic studies suggest that the rate of stroke ipsilateral
to such stenosis is about 1 to 2% annually.
• Ipsilateral carotid endarterectomy was shown to benefit
patients who had 60% or greater diameter reduction of the
artery without ulceration, provided that the perioperative
complication rate was less than 3%.