Stroke Emed
Transcript of Stroke Emed
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Ischemic Stroke
Stroke is characterized by the sudden loss of blood circulation to an area of the brain,
resulting in a corresponding loss of neurologic function. Strokes are classified as either
hemorrhagic or ischemic. Acute ischemic stroke refers to stroke caused by thrombosis or
embolism and is more common than hemorrhagic stroke.
Essential update: New AHA/ASA guidelines for acute stroke treatment
The American Heart Association (AHA) and American Stroke Association (ASA) released
new guidelines for the early management of acute ischemic stroke in January 2013. New
features of the guidelines include a focus on the importance of stroke systems of care, a
recommendation for the use of tissue plasminogen activator (t-PA) in selected patients
presenting within 3 to 4.5 hours of symptom onset, and a recommendation for door-to-needle
times within 60 minutes of hospital arrival in patients eligible for thrombolysis.[1, 2]
Signs and symptoms
Although signs and symptoms of stroke can occur alone, they are more likely to occur incombination. Common stroke signs and symptoms include the following:
Abrupt onset of hemiparesis, monoparesis, or quadriparesis Acute hemisensory loss Complete or partial hemianopia, monocular or binocular visual loss, or diplopia Visual field deficits Diplopia Dysarthria Ataxia Vertigo Nystagmus Aphasia Sudden decrease in the level of consciousness
In younger patients, a history of recent trauma, coagulopathies, illicit drug use (especially
cocaine), migraines, or use of oral contraceptives should be elicited.
SeeClinical Presentationfor more detail.
Diagnosis
With the availability of thrombolytic therapy for acute ischemic stroke in selected patients,
the physician must be able to perform a brief, but accurate, neurologic examination on
patients with suspected stroke syndromes. Essential components of the neurologicexamination include evaluations of the following:
Cranial nerves Motor function Sensory function Cerebellar function Gait Deep tendon reflexes Mental status level of consciousness
The patients skull and spine also should be examined, and signs of meningismus should besought.
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Laboratory studies
Laboratory tests performed in the diagnosis and evaluation of ischemic stroke include the
following:
Complete blood cell count: The CBC count serves as a baseline study and may reveal acause for the stroke (eg, polycythemia, thrombocytosis, thrombocytopenia, leukemia) or
provide evidence of concurrent illness (eg, anemia)
Basic chemistry panel: The chemistry panel serves as a baseline study and may reveal astroke mimic (eg, hypoglycemia, hyponatremia) or provide evidence of concurrent illness
(eg, diabetes, renal insufficiency)
Coagulation studies: Coagulation studies may reveal a coagulopathy and are useful whenthrombolytics or anticoagulants are to be used
Cardiac biomarkers: Cardiac biomarkers are important because of the association ofcerebral vascular disease and coronary artery disease
Toxicology screening: Toxicology screening may assist in identifying intoxicated patientswith symptoms/behavior mimicking stroke syndromes
Pregnancy testing: A urine pregnancy test should be obtained for all women of childbearingage with stroke symptoms; recombinant tissue-type plasminogen activator (rt-PA) is a
pregnancy class C agent
Arterial blood gas analysis: Although infrequent in patients with suspected hypoxemia,arterial blood gas defines the severity of hypoxemia and may be used to detect acid-base
disturbances
Imaging studies
Imaging in ischemic stroke can involve the following modalities:
Several types of magnetic resonance imaging Several types of computed tomography scanning Angiography Ultrasonography Radiology Echocardiography Nuclear imaging
Lumbar puncture
A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the
CT scan is negative but the clinical suspicion remains high
SeeWorkupfor more detail.Management
Ischemic stroke therapies include the following:
Thrombolytic therapy: Thrombolytics restore cerebral blood flow among some patients withacute ischemic stroke and may lead to improvement or resolution of neurologic deficits
Antiplatelet agents: The International Stroke Trial and the Chinese Acute Stroke Trial(CAST) demonstrated modest benefit from the use of aspirin in the setting of acute
ischemic stroke[3, 4]
Mechanical thrombolysis: Involves the endovascular treatment of acute ischemic strokeStroke prevention
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Primary stroke prevention refers to the treatment of individuals with no previous history of
stroke. Measures may include use of the following:
Platelet antiaggregants 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (ie, statins)
ExerciseSecondary prevention refers to the treatment of individuals who have already had a stroke.
Measures may include use of the following:
Platelet antiaggregants Antihypertensives HMG-CoA reductase inhibitors (statins) Lifestyle interventions
SeeTreatmentandMedicationfor more detail.
Image library
Vascular distributions: ACA infarction. Diffusion-weighted image on the left
demonstrates high signal in the paramedian frontal and high parietal regions. The opposite
diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger
ACA infarction involving the left paramedian frontal and posterior parietal regions. There is
also infarction of the lateral temporoparietal regions bilaterally (both MCA distributions),
greater on the left indicating multivessel involvement suggesting emboli.
Background
Stroke is characterized by the sudden loss of blood circulation to an area of the brain,
resulting in a corresponding loss of neurologic function. Also previously called
cerebrovascular accident (CVA) or stroke syndrome, stroke is a nonspecific term
encompassing a heterogeneous group of pathophysiologic causes.
Broadly, however, strokes are classified as either hemorrhagic or ischemic. Acute ischemic
stroke refers to stroke caused by thrombosis or embolism and is more common than
hemorrhagic stroke. (Prior literature indicated that only 8-18% of strokes are hemorrhagic,
but a retrospective review from a stroke center found that 40.9% of 757 strokes included in
the study were hemorrhagic.[5] )
Based on the system of categorizing stroke developed in the multicenter Trial of Org 10172
in Acute Stroke Treatment (TOAST), ischemic strokes may be divided into the following 3
major subtypes[6] :
Large artery infarction: Thrombotic strokes are caused by in situ occlusions onatherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically
proximal to major branches.
Small-vessel, or lacunar, infarction Cardioembolic infarction: Cardiogenic emboli are a common source of recurrent stroke.
They may account for up to 20% of acute strokes and have been reported to have the
highest 1-month mortality. (See Pathophysiology.)
The National Institute of Neurologic Disorders and Stroke (NINDS) recombinant tissue-type
plasminogen activator (rt-PA) stroke study group first reported that the early administration
of rt-PA benefited carefully selected patients with acute ischemic stroke.[7] The trials
outcome led to the long-standing goal of t-PA administration within a 3-hour window for a
patient deemed likely to benefit from thrombolytic intervention. Encouraged by this
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breakthrough study and the subsequent approval by the US Food and Drug Administration
(FDA) of the use of t-PA in acute ischemic stroke, many medical professionals now consider
acute ischemic stroke to be a medical emergency that may be amenable to treatment.
Thrombolytic therapyadministered between 3 and 4.5 hours after the onset of symptoms was
found to be efficacious in improving neurologic outcomes in the European Cooperative AcuteStroke Study III (ECASS III), suggesting a wider time window for the administration of
thrombolytics.[8] Based on this and other data, in May 2009, the American Heart Association
and the American Stroke Association guidelines for the administration of rt-PA were revised
to expand the treatment window from 3 to 4.5 hours.[9] This indication has not yet been FDA
approved.
Understanding of the pathophysiology, clinical presentation, and evaluation of the stroke
patient is essential, as is knowledge of the therapeutic armamentarium currently available to
treat acute ischemic stroke, which includes supportive care, treatment of neurologic
complications, antiplatelet therapy, glycemic control, blood pressure control, prevention of
hyperthermia, and thrombolytic therapy.
Anatomy
The brain is the most metabolically active organ in the body. While representing only 2% of
the body's mass, it requires 15-20% of the total resting cardiac output to provide the
necessary glucose and oxygen for its metabolism. See theCardiac Outputcalculator.
Knowledge of cerebrovascular arterial anatomy and the territories supplied by each is useful
in determining which vessels are involved in acute stroke. Atypical patterns that do not
conform to a vascular distribution may indicate a diagnosis other than ischemic stroke, such
as venous infarction.
Arterial distributions
The cerebral hemispheres are supplied by 3 paired major arteries, specifically, the anterior,
middle, and posterior cerebral arteries.
The anterior and middle cerebral arteries carry the anterior circulation and arise from the
supraclinoid internal carotid arteries. The anterior cerebral artery (ACA) supplies the medial
portion of the frontal and parietal lobes and anterior portions of basal ganglia and anterior
internal capsule. The middle cerebral artery (MCA) supplies the lateral portions of the frontal
and parietal lobes, as well as the anterior and lateral portions of the temporal lobes, and gives
rise to perforating branches to the globus pallidus, putamen and internal capsule.
The posterior cerebral arteries arise from the basilar artery and carry the posterior circulation.The posterior cerebral artery (PCA) gives rise to perforating branches that supply the thalami
and brainstem and the cortical branches to the posterior and medial temporal lobes and
occipital lobes. The cerebellar hemispheres are supplied inferiorly by the posterior inferior
cerebellar artery (PICA) arising from the vertebral artery, superiorly by the superior
cerebellar artery, and anterolaterally by the anterior inferior cerebellar artery (AICA) from
the basilar artery.
Pathophysiology
Acute ischemic strokes are the result of vascular occlusion secondary to thromboembolic
disease (see Etiology). Ischemia results in cell hypoxia and depletion of cellular adenosine
triphosphate (ATP). Without ATP, energy failure results in an inability to maintain ionic
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gradients across the cell membrane and cell depolarization. With an influx of sodium and
calcium ions and passive inflow of water into the cell, cytotoxic edema results.[10, 11, 12]
Ischemic core and penumbra
An acute vascular occlusion produces heterogeneous regions of ischemia in the affected
vascular territory. The quantity of local blood flow is made up of any residual flow in themajor arterial source and the collateral supply, if any.
Regions of the brain with CBF lower than 10 mL/100g of tissue/min are referred to
collectively as the core, and these cells are presumed to die within minutes of stroke onset.
Zones of decreased or marginal perfusion (CBF < 25 mL/100g of tissue/min) are collectively
called the ischemic penumbra. Tissue in the penumbra can remain viable for several hours
because of marginal tissue perfusion.
Ischemic cascade
On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted andmembrane ion-transport systems fail. The resulting influx of calcium leads to the release of a
number of neurotransmitters, including large quantities of glutamate, which in turn
activatesN-methyl-D-aspartate (NMDA) and other excitatory receptors on other neurons.
These neurons then become depolarized, causing further calcium influx, further glutamate
release, and local amplification of the initial ischemic insult. This massive calcium influx also
activates various degradative enzymes, leading to the destruction of the cell membrane and
other essential neuronal structures.[13]
Free radicals, arachidonic acid, and nitric oxide are generated by this process, which leads to
further neuronal damage.
Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown ofthe blood-brain barrier occurring within 4-6 hours after infarction. Following the barriers
breakdown, proteins and water flood into the extracellular space, leading to vasogenic edema.
Vasogenic edema produces greater levels of brain swelling and mass effect that peaks at 3-5
days and resolves over the next several weeks with resorption of water and proteins.[14, 15]
Within hours to days after a stroke, specific genes are activated, leading to the formation of
cytokines and other factors that, in turn, cause further inflammation and microcirculatory
compromise.[13] Ultimately, the ischemic penumbra is consumed by these progressive insults,
coalescing with the infarcted core, often within hours of the onset of the stroke.
Infarction results in the death of astrocytes as well as the supporting oligodendroglia andmicroglia cells. The infarcted tissue eventually undergoes liquefaction necrosis and is
removed by macrophages with the development of parenchymal volume loss. A well-
circumscribed region of cerebrospinal fluidlike low density is eventually seen, consisting of
encephalomalacia and cystic change. The evolution of these chronic changes may be seen in
the weeks to months following the infarction.
Hemorrhagic transformation of ischemic stroke
Hemorrhagic transformation represents the conversion of a bland infarction into an area of
hemorrhage. This is estimated to occur in 5% of uncomplicated ischemic strokes, in the
absence of thrombolytics. Hemorrhagic transformation is not always associated with
neurologic decline and ranges from small petechial hemorrhages to hematomas requiringevacuation.
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Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically
injured tissue, either from recanalization of an occluded vessel or from collateral blood
supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of
the blood-brain barrier, red blood cells extravasate from the weakened capillary bed
producing petechial hemorrhage or more frank intraparenchymal hematoma.[10, 16, 17]
Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days post ictus,
usually within the first week. It is more commonly seen following cardioembolic strokes and
is more likely with larger infarct size.[10, 18, 7]Hemorrhagic transformation is also more likely
following administration of t-PA, with noncontrast computed tomography (NCCT) scanning
demonstrating areas of hypodensity.[19, 20, 21]
Poststroke cerebral edema and seizures
Although significant cerebral edema can occur after anterior circulation ischemic stroke, it is
thought to be somewhat rare (10-20%).[22] Edema and herniation are the most common causes
of early death in patients with hemispheric stroke.
Seizures occur in 2-23% of patients within the first days after stroke.[22] A fraction of patients
who have experienced stroke develop chronic seizure disorders.
Etiology
Ischemic strokes result from events that limit or stop blood flow, such as extracranial or
intracranial thrombosis embolism, thrombosis in situ, or relative hypoperfusion. As blood
flow decreases, neurons cease functioning, and irreversible neuronal ischemia and injury
begin at blood flow rates of less than 18 mL/100 g of tissue/min.
Risk factors
Risk factors for ischemic stroke include 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 the following:
Age Race Sex Ethnicity History of migraine headaches Sickle cell disease Fibromuscular dysplasia 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
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Lifestyle issues - Excessive alcohol intake, tobacco use, illicit drug use, obesity, physicalinactivity
Oral contraceptive useAmong the types of cardiac disease that increase stroke risk are 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.
TIA is a transient neurologic deficit with no evidence of an ischemic lesion on neuroimaging.
Roughly 80% resolve within 60 minutes.[23]
TIA can result from the aforementioned mechanisms of stroke. Data suggest that roughly
10% of patients with TIA suffer stroke within 90 days and half of these patients suffer stroke
within 2 days.[24, 25]
Genetic and inflammatory mechanisms
Evidence continues to accumulate to suggest important roles for inflammation and genetic
factors in the process ofatherosclerosisand, specifically, in stroke. According to the currentparadigm, atherosclerosis is not a bland cholesterol storage disease, as previously thought,
but a dynamic, chronic, inflammatory condition caused by a response to endothelial injury.
Traditional risk factors, such as oxidized low-density lipoprotein (LDL) and smoking,
contribute to this injury. It has been suggested, however, that infections may also contribute
to endothelial injury and atherosclerosis.
Host genetic factors, moreover, may modify the response to these environmental challenges,
although inherited risk for stroke is likely multigenic. Even so, specific single-gene disorders
with stroke as a component of the phenotype demonstrate the potency of genetics in
determining stroke risk.
Flow disturbances
Stroke symptoms can result from inadequate cerebral blood flow due to decreased blood
pressure (and specifically, decreased cerebral perfusion pressure) or as a result of
hematologic hyperviscosity due to sickle cell disease or other hematologic illnesses, such as
multiple myeloma and polycythemia vera. In these instances, cerebral injury may occur in the
presence of damage to other organ systems.
Large-artery occlusion
Large-artery occlusion typically results from embolization of atherosclerotic debris
originating from the common or internal carotid arteries or from a cardiac source. A smaller
number of large-artery occlusions may arise from plaque ulceration and in situ thrombosis.Large-vessel ischemic strokes more commonly affect the MCA territory with the ACA
territory affected to a lesser degree.
Lacunar strokes
Lacunar strokes represent 13-20% of all ischemic strokes. They occur when the penetrating
branches of the 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 the following:
Microatheroma
Lipohyalinosis
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Fibrinoid necrosis secondary to hypertension or vasculitis Hyaline arteriosclerosis Amyloid angiopathy
The great majority are related to hypertension.
Embolic strokesCardiogenic emboli may account for up to 20% of acute strokes.
Emboli may arise from the heart, the extracranial arteries, or, rarely, the right-sided
circulation (paradoxical emboli) with subsequent passage through a patent foramen ovale.
The sources of cardiogenic emboli include the following:
Valvular thrombi (eg, inmitral stenosisorendocarditisor from use of a prosthetic valve) Mural thrombi (eg, inmyocardial infarction[MI],atrial fibrillation[AF],dilated
cardiomyopathy, or severe congestive heart failure [CHF])
Atrial myxomaMI is associated with a 2-3% incidence of embolic strokes, of which 85% occur in the firstmonth after MI.[26] Embolic strokes tend to have a sudden onset, and neuroimaging may
demonstrate previous infarcts in several vascular territories or calcific emboli.
Risk factors include atrial fibrillation and recent cardiac surgery. Cardioembolic strokes may
be isolated, multiple and in a single hemisphere, or scattered and bilateral; the latter 2 types
indicate multiple vascular distributions and are more specific for cardioembolism. Multiple
and bilateral infarcts can be the result of embolic showers or recurrent emboli. Other
possibilities for single and bilateral hemispheric infarctions include emboli originating from
the aortic arch and diffuse thrombotic or inflammatory processes that can lead to multiple
small-vessel occlusions.
Thrombotic strokes
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. Arterial stenosis can cause turbulent blood
flow, which can increase the risk for thrombus formation, atherosclerosis (ie, ulcerated
plaques), and platelet adherence; all cause the formation of blood clots that either embolize or
occlude the artery.
Intracranial atherosclerosis may be the cause in patients with widespread atherosclerosis. In
other patients, especially younger patients, other causes should be considered, including the
following[29, 10] :
Hypercoagulable states (eg, antiphospholipid antibodies, protein C deficiency, protein S
deficiency, pregnancy)
Sickle cell disease Fibromuscular dysplasia Arterial dissections Vasoconstriction associated with substance abuse
Watershed infarcts
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Vascular watershed, or border-zone, infarctions occur at the most distal areas between arterial
territories. They are believed to be secondary to embolic phenomenon or due to severe
hypoperfusion, such as in carotid occlusion or prolonged hypotension.
Epidemiology
Stroke is the leading cause of disability and the third leading cause of death in the UnitedStates.[33]
More than 700,000 persons per year suffer a first-time stroke in the United States, with 20%
of these individuals dying within the first year after the stroke. If current trends continue, this
number is projected to reach 1 million per year by the year 2050.[34]
The global incidence of stroke is unknown.
Stroke incidence by race and sex
In the United States, blacks have an age-adjusted risk of death from stroke that is 1.49 times
that of whites.[35]
Hispanics have a lower overall incidence of stroke than whites and blacks but more frequent
lacunar strokes and stroke at an earlier age.
Men are at higher risk for stroke than women; white males have a stroke incidence of 62.8
per 100,000, with death being the final outcome in 26.3% of cases, while women have a
stroke incidence of 59 per 100,000 and a death rate of 39.2%.
Stroke and age
Although stroke often is considered a disease of elderly persons, one third of strokes occur in
persons younger than 65 years.[34] Risk of stroke increases with age, especially in patients
older than 64 years, in whom 75% of all strokes occur.
Prognosis
The prognosis after acute ischemic stroke varies greatly, depending on the stroke severity and
on the patients premorbid condition, age, and poststroke complications.[6]
Some patients experience hemorrhagic transformation of their infarct (See Pathophysiology).
This is estimated to occur in 5% of uncomplicated ischemic strokes, in the absence of
thrombolytics. Hemorrhagic transformation is not always associated with neurologic decline
and ranges from small petechial hemorrhages to hematomas requiring evacuation.
In the Framingham and Rochester stroke studies, the overall mortality rate at 30 days afterstroke was 28%, the mortality rate at 30 days after ischemic stroke was 19%, and the 1-year
survival rate for patients with ischemic stroke was 77%.
In the United States, 20% of individuals die within the first year after a first-time stroke, as
previously mentioned.
Cardiogenic emboli are associated with the highest 1-month mortality in patients with acutestroke.
In stroke survivors from the Framingham Heart Study, 31% needed help caring for
themselves, 20% needed help when walking, and 71% had impaired vocational capacity in
long-term follow-up.
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The presence of CT scan evidence of infarction early in presentation has been associated with
poor outcome and with an increased propensity for hemorrhagic transformation after
thrombolytics.[7, 36, 37]
Acute ischemic stroke has been associated with acute cardiac dysfunction and arrhythmia,
which then correlate with worse functional outcome and morbidity at 3 months.Data suggest that severe hyperglycemia is independently associated with poor outcome and
reduced reperfusion in thrombolysis, as well as extension of the infarcted territory.[38, 39, 40]
To see complete information on Motor Recovery in Stroke, please go to the main article by
clickinghere.
Patient Education
Public education must involve all age groups. Incorporating stroke into basic life support
(BLS) and cardiopulmonary resuscitation (CPR) curricula is just one way to reach a younger
audience. Avenues to reach an audience with a higher stroke risk include using local
churches, employers, and senior organizations to promote stroke awareness.
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 1 side of the body Sudden confusion Sudden difficulty in speaking or understanding Sudden deterioration of vision in 1 or both eyes Sudden difficulty in walking, dizziness, and loss of balance or coordination
Sudden, severe headache with no known cause
History
A focused medical history for patients with ischemic stroke 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 (see Etiology). Consider stroke in any patient presenting with acute neurologic
deficit or any alteration in level of consciousness. Common signs of stroke include the
following:
Acute hemiparesis or hemiplegia Acute hemisensory loss Complete or partial hemianopia, monocular or binocular visual loss, or diplopia Dysarthria or aphasia Ataxia, vertigo, or nystagmus Sudden decrease in consciousness
In younger patients, elicit a history of recent trauma, coagulopathies, illicit drug use
(especially cocaine), migraines, or use of oral contraceptives.
Establishing the time at which the patient was last without stroke symptoms is especially
critical when thrombolytic therapy is an option. If the patient awakens with symptoms, then
the time of onset is defined as the time at which the patient was last seen to be without
symptoms. Family members, coworkers, and bystanders may be required to help establish the
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exact time of onset, especially in right hemispheric strokes accompanied by neglect or left
hemispheric strokes with aphasia.
Physical Examination
The goals of the physical examination include detecting extracranial causes of stroke
symptoms, distinguishing stroke from stroke mimics, determining and documenting for futurecomparison the degree of deficit, and localizing the lesion.
The physical examination always includes a careful head and neck examination for signs of
trauma, infection, and meningeal irritation.
Stroke should be considered in any patient presenting with an acute neurologic deficit (focal
or global) or altered level of consciousness. No historical feature distinguishes ischemic from
hemorrhagic stroke, although nausea, vomiting, headache, and change in level of
consciousness are more common in hemorrhagic strokes.
Common symptoms of stroke include the following:
Abrupt onset of hemiparesis, monoparesis, or quadriparesis Hemisensory deficits Monocular or binocular visual loss Visual field deficits Diplopia Dysarthria Ataxia Vertigo Aphasia Sudden decrease in the level of consciousness
Although such symptoms can occur alone, they are more likely to occur in combination.
A careful search for the cardiovascular causes of stroke requires examination of the ocular
fundi (retinopathy, emboli, hemorrhage), heart (irregular rhythm, murmur, gallop), and
peripheral vasculature (palpation of carotid, radial, and femoral pulses, auscultation for
carotid bruit).
Patients with a decreased level of consciousness should be assessed to ensure that they are
able to protect their airway.
The physical examination must encompass all of the major organ systems, starting with the
airway, breathing, and circulation (ABC) and the vital signs. Patients with stroke, especially
hemorrhagic stroke, can clinically deteriorate quickly; therefore, constant reassessment iscritical. Ischemic strokes, unless large or involving the brainstem, do not tend to cause
immediate problems with airway patency, breathing, or circulation compromise. On the other
hand, patients with intracerebral or subarachnoid hemorrhage frequently require intervention
for airway protection and ventilation.
Vital signs, while nonspecific, can point to impending clinical deterioration and may assist in
narrowing the differential diagnosis. Many patients with stroke are hypertensive at baseline,
and their blood pressure may become more elevated after stroke. While hypertension at
presentation is common, blood pressure decreases spontaneously over time in most patients.
Acutely lowering blood pressure has not proven to be beneficial in these stroke patients in the
absence of signs and symptoms of associated malignant hypertension, acute myocardialinfarction, CHF, or aortic dissection.
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Head and neck examination
A careful examination of the head and neck is essential. Contusions, lacerations, and
deformities may suggest trauma as the etiology for the patient's symptoms. Auscultation of
the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.
Cardiac examination
Cardiac arrhythmias, such as atrial fibrillation, are found commonly in patients with stroke.
Similarly, strokes may occur concurrently with other acute cardiac conditions, such as acute
myocardial infarction and acute CHF; thus, auscultation for murmurs and gallops is
recommended.
Examination of the extremities
Carotid or vertebrobasilar dissections and, less commonly, thoracic aortic dissections may
cause ischemic stroke. Unequal pulses or blood pressures in the extremities may reflect the
presence of aortic dissections.
Neurologic examination
With the availability of thrombolytic therapy for acute ischemic stroke in selected patients,
the physician must be able to perform a brief, but accurate, neurologic examination on
patients with suspected stroke syndromes. The goals of the neurologic examination include
the following:
Confirming the presence of a stroke syndrome (to be defined further by cranial computedtomography [CT] scanning)
Distinguishing stroke from stroke mimics Establishing a neurologic baseline should the patient's condition improve or deteriorate
Essential components of the neurologic examination include the evaluation of cranial nerves,motor function, sensory function, cerebellar function, gait, and deep tendon reflexes, as well
as of mental status and level of consciousness. The skull and spine also should be examined,
and signs of meningismus should be sought.
Central facial weakness from a stroke should be differentiated from the peripheral weakness
ofBell palsy. With peripheral lesions (Bell palsy), the patient is unable to lift the eyebrows,
wrinkle the forehead, or or close the eye on the affected side.
A useful tool in quantifying neurological impairment is the National Institutes of Health
Stroke Scale (NIHSS). The NIHSS (see Table 2, below and theNIH Stroke Scorecalculator)
is used mostly by stroke teams. It enables the consultant to rapidly determine the severity and
possible location of the stroke. A patient's score on the NIHSS is strongly associated with
outcome, and it can help to identify those patients who are likely to benefit from thrombolytic
therapy and those who are at higher risk of developing hemorrhagic complications of
thrombolytic use.
This scale is easily used and focuses on the following 6 major areas of the neurologic
examination:
level of consciousness Visual function Motor function Sensation and neglect Cerebellar function
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LanguageThe NIHSS is a 42-point scale, with minor strokes usually being considered to have a score
less than 5. An NIHSS score greater than 10 correlates with an 80% likelihood of visual flow
deficits on angiography. However, discretion must be used in assessing the magnitude of the
clinical deficit; for instance, if a patient's only deficit is being mute, the NIHSS score will be
3. Additionally, the scale does not measure some deficits associated with posterior circulationstrokes (ie, vertigo, ataxia).
Middle cerebral artery stroke
MCA occlusion commonly produces contralateral hemiparesis, contralateral hypesthesia,
ipsilateral hemianopsia, and gaze preference toward the side of the lesion. Agnosia is
common, and receptive or expressive aphasia may result if the lesion occurs in the dominant
hemisphere. Neglect, inattention, and extinction of double simultaneous stimulation mayoccur in nondominant hemisphere lesions. Since the MCA supplies the upper extremity
motor strip, weakness of the arm and face is usually worse than that of the lower limb.
Anterior cerebral artery stroke
ACA occlusions primarily affect frontal lobe function and can result in disinhibition and
speech perseveration, producing primitive reflexes (eg, grasping, sucking reflexes), altered
mental status, impaired judgment, contralateral weakness (greater in legs than arms),
contralateral cortical sensory deficits gait apraxia, and urinary incontinence.
Posterior cerebral artery stroke
PCA occlusions affect vision and thought, producing contralateral homonymoushemianopsia, cortical blindness, visual agnosia, altered mental status, and impaired memory.
Vertebrobasilar artery occlusions are notoriously difficult to detect because they cause a wide
variety of cranial nerve, cerebellar, and brainstem deficits. These include the following:
Vertigo Nystagmus Diplopia Visual field deficits Dysphagia
Dysarthria Facial hypesthesia Syncope Ataxia
A hallmark of posterior circulation stroke is that there are crossed findings: ipsilateral cranial
nerve deficits and contralateral motor deficits. This is contrasted to anterior stroke, which
produces only unilateral findings.
Lacunar stroke
Lacunar strokes result from occlusion of the small, perforating arteries of the deep subcortical
areas of the brain. The infarcts are generally from 2-20 mm in diameter. The most common
lacunar syndromes include pure motor, pure sensory, and ataxic hemiparetic strokes. By
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virtue of their small size and well-defined subcortical location, lacunar infarcts do not lead to
impairments in cognition, memory, speech, or level of consciousness.
Treatment
Thrombolytic Therapy
Thrombolytics restore cerebral blood flow among some patients with acute ischemic stroke
and may lead to improvement or resolution of neurologic deficits. Unfortunately,
thrombolytics can also cause symptomatic intracranial hemorrhage, defined as radiographic
evidence of hemorrhage combined with escalation of the NIHSS score by 4 or more points
(see theNIH Stroke Scorecalculator). Therefore, if the patient is a candidate for thrombolytic
therapy, a thorough review of the inclusion and exclusion criteria must be performed. The
exclusion criteria largely focus on identifying risk of hemorrhagic complication associated
with thrombolytic use.
While streptokinase and rt-PA have been shown to benefit patients with acute MI, only
alteplase (rt-PA) has been shown to benefit selected patients with acute ischemic stroke.
In May 2009, the American Heart Association/American Stroke Association (AHA/ASA)
guidelines for the administration of rt-PA following acute stroke were revised to expand the
window of treatment from 3 hours to 4.5 hours to provide more patients with an opportunity
to receive benefit from this effective therapy.[8, 9, 61] Eligibility criteria for treatment in the 3-
4.5 hours after acute stroke are similar to those for treatment at earlier time periods, with any
1 of the following additional exclusion criteria:
Patients older than 80 years All patients taking oral anticoagulants are excluded regardless of the international
normalized ratio (INR)
Patients with baseline NIHSS greater than 25 Patients with a history of stroke and diabetes
Caution should be exercised in the administration of rt-PA to patients with major deficits.
Patients with evidence of low attenuation (edema or ischemia) involving more than a third of
the distribution of the MCA on their initial NCCT scan are less likely to have favorable
outcome after thrombolytic therapy and are thought to be at higher risk for hemorrhagic
transformation of their ischemic stroke.[36] In addition to the risk of symptomatic intracranial
hemorrhage (6.4% in the NINDS trial), other complications include potentially
hemodynamically significant hemorrhage and angioedema or allergic reactions.[22]
Streptokinase has not been shown to benefit patients with acute ischemic stroke, but it has
been shown to increase their risk of intracranial hemorrhage and death.
Researchers have studied the use of transcranial ultrasound as a means of assisting rt-PA in
thrombolysis. By delivering mechanical pressure waves to the thrombus, ultrasound can
theoretically expose more of its surface to the circulating thrombolytic agent. Further
research is necessary to determine the exact role of transcranial Doppler ultrasound in
assisting thrombolytics in acute ischemic stroke.
No human trials comparing the IV versus intra-arterial administration of thrombolytics exist.
Theoretic advantages to intra-arterial delivery may include the possibility that higher local
concentrations of thrombolytic would allow lower total doses of the agent (and theoretically
less risk of systemic bleed) and a longer therapeutic window; however, the longer time to
administration via the intra-arterial approach versus the IV approach may mitigate some of
this advantage.
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For more information, seeThrombolytic Therapy.
For more information, seeReperfusion Injury in Stroke.
Antiplatelet Agents
The International Stroke Trial and the Chinese Acute Stroke Trial (CAST) demonstrated
modest benefit from the use of aspirin in the setting of acute ischemic stroke. The
International Stroke Trial randomized 20,000 patients within 48 hours of stroke onset to
treatment with aspirin 325 mg, subcutaneous heparin in 2 different dose regimens, aspirin
with heparin, and a placebo. The study found that aspirin therapy reduced the risk of early
stroke recurrence.[3, 4]
CAST evaluated 21,106 patients and had a 4-week mortality reduction of 3.3% contrasted to
3.9%. A separate study also found that the combination of aspirin and lowmolecular-weight
heparin did not significantly improve outcomes.[3]
The early initiation of aspirin plus extended-release dipyridamole is likely to be as safe and
effective in preventing disability as is later initiation after 7 days following stroke onset,according to a German study. The studys authors attempted to assess the precise time to
initiate dipyridamole following ischemic stroke or TIA.[62] Patients from 46 stroke units who
presented with an NIHSS score of 20 or less were randomly assigned to receive aspirin 25 mg
plus extended-release dipyridamole 200 mg bid (early dipyridamole regimen) (n=283) or
aspirin monotherapy (100 mg once daily) for 7 days (n=260). Therapy in either group was
initiated within 24 hours of stroke onset.
After 2 weeks, all patients received aspirin plus dipyridamole for up to 90 days. At day 90,
154 (56%) patients in the early dipyridamole group and 133 (52%) in the aspirin plus later
dipyridamole group had no or mild disability (P= .45).
Other antiplatelet agents are also under evaluation for use in the acute presentation of
ischemic stroke. In a preliminary pilot study, abciximab was given within 6 hours to establish
a safety profile. A trend toward improved outcome at 3 months for the treatment versus the
placebo group was noted.[63] Further clinical trials are necessary.
Neuroprotective Agents
Despite very promising results in several animal studies, as of yet no single neuroprotective
agent in ischemic stroke is supported by randomized, placebo-controlled human studies.
Nevertheless, substantial research is underway evaluating different neuroprotective strategies,
including hypothermia.
For more information, seeNeuroprotective Agents in Stroke.
Mechanical Thrombolysis
Studies have evaluated the efficacy of mechanical clot disruption in the setting of acute
stroke. In most cases, these technologies were used in combination with thrombolysis. In an
investigation by Berlis et al, mechanical disruption via an endovascular photoacoustic device
was found to be more effective than thrombolysis alone in recanalization rates.[64]
There are currently 2 FDA-approved devices for the endovascular treatment of acute
ischemic stroke: the Concentric Retriever, which is mainly a grasping device, and the
Penumbra device, which employs an aspiration function to remove clots.[65, 66, 67] The
Penumbra trial demonstrated 82% recanalization in patients when using the aspirationfunction of the Penumbra device.
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Successful recanalization occurred in 12 of 28 patients in the Mechanical Embolus Retrieval
in Cerebral Ischemia (MERCI) 1 pilot trial, a study of the Merci Retrieval System.[68]
In a second MERCI study, recanalization was achieved in 48% of those in which the device
was deployed. Clot was successfully retrieved from all major cerebral arteries; however, the
recanalization rate for the MCA was lowest. A further study of clot extraction, the Prolyse inAcute Cerebral Thromboembolism II (PROACT II) study, identified a recanalization rate of
66%.[69, 70]
The Multi MERCI trial used the newer generation Concentric retrieval device (L5).
Recanalization was demonstrated in approximately 55% of patients who did not receive t-PA
and in 68% of those for whom t-PA was given in a group of patients with acute ischemic
stroke presenting within 8 hours of onset of symptoms. Seventy-three percent of patients who
failed IV t-PA therapy had recanalization following mechanical embolectomy.[71] However,
based on these results, the FDA has cleared the use of the MERCI device in patients who are
either ineligible for or who have failed IV thrombolytics.
According to the 2011 AHA/ASA statement on CVT, evidence is insufficient to drawconclusions about the value of endovascular thrombolysis in patients with CVT. For that
reason, the statement recommends this therapy only in patients with progressive neurological
deterioration that persists despite medical treatment.[44]
For more information, seeMechanical Thrombolysis in Acute Stroke.
For more information, seeCerebral Revascularization.
Fever Control
Antipyretics are indicated for febrile stroke patients, since hyperthermia accelerates ischemic
neuronal injury. Substantial experimental evidence suggests that mild brain hypothermia isneuroprotective. The use of induced hypothermia is currently being evaluated in phase I
clinical trials.[72, 73, 74]
High body temperature in the first 12-24 hours after stroke onset has been associated with
poor functional outcome. Results from the Paracetamol (Acetaminophen) In Stroke (PAIS)
trial did not support the routine use of high-dose acetaminophen in patients with acute stroke.
The study assessed whether early treatment with paracetamol improves functional outcome in
patients with acute stroke by reducing body temperature and preventing fever. Patients
(n=1400) were randomly assigned to receive acetaminophen (6 g daily) or placebo within 12
hours of symptom onset. After 3 months, improvement on the modified Rankin scale was not
beyond what was expected.[75]
Cerebral Edema Control
Significant cerebral edema after ischemic stroke is thought to be somewhat rare (10-20%);
maximum severity of edema is reached 72-96 hours after the onset of stroke.
Early indicators of ischemia on presentation and on NCCT scans are independent indicators
of potential swelling and deterioration. Mannitol and other therapies to reduce ICP may be
used in emergency situations, although their usefulness in swelling secondary to ischemic
stroke is unknown. No evidence exists supporting the use of corticosteroids to decrease
cerebral edema in acute ischemic stroke. Prompt neurosurgical assistance should be sought
when indicated.[22]
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Patient position, hyperventilation, hyperosmolar therapy, and, rarely, barbiturate coma may
be used, as in patients with increased ICP secondary to closed head injury. Hemicraniectomy
has shown to decrease mortality and disability among patients with large hemispheric
infarctions associated with life-threatening edema.[76, 77, 78, 79]
Seizure ControlSeizures occur in 2-23% of patients within the first days after stroke. Although seizure
prophylaxis is not indicated, prevention of subsequent seizures with standard antiepileptic
therapy is recommended.[22]
The 2011 AHA/ASA CVT statement notes a lack of clinical trials on the use of
anticonvulsants to control seizures, which occur in 37% of adults, 48% of children, and 71%
of newborns who present with CVT. Therefore, opinions on their use vary greatly. However,
because seizures increase the risk of anoxic damage, anticonvulsant treatment after even a
single seizure is reasonable.[44]
Post-ischemia strokes are usually focal, but they may be generalized. A fraction of patients
who have experienced stroke develop chronic seizure disorders. Seizures secondary to
ischemic stroke should be managed in the same manner as other seizure disorders that arise
as a result of neurologic injury.[22]
Acute Decompensation or Escalation
In the case of the rapidly decompensating patient or the patient with deteriorating neurologic
status, reassessment of ABCs as well as hemodynamics and reimaging are indicated. Many
patients who develop hemorrhagic transformation or progressive cerebral edema will
demonstrate acute clinical decline. Rarely, a patient may have escalation of symptoms
secondary to increased size of the ischemic penumbra. Some advocate resetting the time
window to zero in this circumstance and encourage consideration of reperfusion strategies.Anticoagulation and Prophylaxis
Heparin is known to prolong the lytic state caused by t-PA. Currently, data are inadequate to
justify the utilization of heparin or other anticoagulants in the acute management of patients
with ischemic stroke. Patients with embolic stroke who have another indication for
anticoagulation (eg, atrial fibrillation) may be placed on anticoagulation therapy with the goal
of preventing further embolic disease; however, the potential beneficial effects from that
decision must be weighted against the risk of hemorrhagic transformation.[22]
Immobilized stroke patients who are not receiving anticoagulants, such as IV heparin or an
oral anticoagulant, may benefit from the administration of low-dose, subcutaneous
unfractionated or lowmolecular-weight heparin, which reduces the risk of deep venous
thrombosis.[22]
For more information, seeStroke Anticoagulation and Prophylaxis.
Induced Hypothermia
Hypothermia is fast becoming the standard of care for the ongoing treatment of patients
surviving cardiac arrest due to ventricular tachycardia or ventricular fibrillation. However, no
major clinical study has demonstrated a role for hypothermia in the early treatment of
ischemic stroke.[22]
Carotid Endarterectomy
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Many surgical and endovascular techniques have been studied in the treatment of acute
ischemic stroke. Carotid endarterectomy has been used with some success in the acute
management of internal carotid artery occlusions, but no evidence supports its use in acute
stroke.
Stroke PreventionPrimary prevention refers to the treatment of individuals with no previous history of stroke.
Measures may include the use of platelet antiaggregants; 3-hydroxy-3-methylglutaryl
coenzyme A (HMG-CoA) reductase inhibitors (ie, statins); and exercise. In February 2011,
AHA/ASA guidelines for the primary prevention of stroke were published. The guideline
emphasizes the importance of lifestyle changes to reduce well-documented modifiable risk
factors, citing an 80% lower risk of a first stroke in people who follow a healthy lifestyle
compared with those who do not.[80]
Secondary prevention refers to the treatment of individuals who have already had a stroke.
Measures may include the use of platelet antiaggregants, antihypertensives, HMG-CoA
reductase inhibitors (statins), and lifestyle interventions.
Smoking cessation, blood pressure control, diabetes control, a low-fat diet, weight loss, and
regular exercise should be encouraged as strongly as the medications described above.
Written prescriptions for exercise and medications for smoking cessation (nicotine patch,
bupropion, varenicline) increase the likelihood of success with these interventions.
In addition to these well-documented factors, the 2011 AHA/ASA guidelines for primary
stroke prevention indicate that it is reasonable to avoid exposure to environmental tobacco
smoke despite a lack of stroke-specific data.
The use of aspirin for primary stroke prevention is not recommended for persons at low risk.
Aspirin is recommended for this purpose only in persons with at least a 6-10% risk ofcardiovascular events over 10 years.[80]
For patients with stroke risk due to asymptomatic carotid artery stenosis, the 2011 AHA/ASA
primary prevention guidelines state that older studies that showed revascularization surgery
as more beneficial than medical treatment may now be obsolete due to improvements in
medical therapies. Therefore, individual patient comorbidities, life expectancy, and
preferences should determine whether medical treatment alone or carotid revascularization is
selected.[80]
Atrial fibrillation is a major risk factor for stroke. The 2011 ACC Foundation
(ACCF)/AHA/Heart Rhythm Society (HRS) atrial fibrillation guideline update on dabigatran
states that the new anticoagulant dabigatran is useful as an alternative to warfarin in patients
with atrial fibrillation who do not have a prosthetic heart valve or hemodynamically
significant valve disease.[81]
The 2011 AHA/ASA primary stroke prevention guideline recommends that EDs screen for
AF and assess patients for anticoagulation therapy if AF is found.[80]
For patients with atrial fibrillation after stroke or TIA, the 2010 AHA/ASA secondary stroke
prevention guideline is in accord with the standard recommendation of warfarin, with aspirin
as an alternative for patients who cannot take oral anticoagulants. However, clopidogrel
should not be used in combination with aspirin for such patients because the bleeding risk of
the combination is comparable to that of warfarin. The guideline states that the benefit ofwarfarin after stroke or TIA in patients without atrial fibrillation has not been established.[82]
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The 2011 AHA/ASA guideline recommends ED-based smoking cessation interventions, and
considers it reasonable for EDs to screen patients for hypertension and drug abuse.[80]
Specialized Stroke Centers
Given the multitude of factors that go into the care of a patient with acute stroke, the concept
of the specialized stroke center has evolved. The Brain Attack Coalition providedrecommendations for the establishment of 2 tiers of stroke centers: primary stroke centers
(PSCs) and comprehensive stroke centers (CSCs).[22] The Joint Commission for the
Accreditation of Hospital Organizations (JCAHO) now provides accreditation for PSC, and
efforts to establish the requirements that distinguish CSC are currently ongoing.
The PSC is designed to maximize the timely provision of stroke-specific therapy, including
the administration of rt-PA, and is also capable of providing care to patients with
uncomplicated stroke. The CSC shares the commitment that the PSC has to acute delivery of
rt-PA and also provides care to patients with hemorrhagic stroke and intracranial hemorrhage
and all patients with stroke requiring ICU level of care.[22]
Once patients have been identified as potential stroke patients, their ED evaluation must be
fast-tracked to allow for the completion of required laboratory tests and requisite noncontrast
head CT scanning, as well as the notification and involvement of neurologic consultation.
These requirements have led to the development of "stroke codes" or "stroke activations" in
which EMS crews have been trained to identify possible stroke patients and arrange for their
speedy, preferential transport to a PSC or CSC.
Additionally, Stroke Centers should have personnel versed at monitoring stroke vital signs,
which include the following:
Blood pressure Glucose levels Temperature Oxygenation Change in neurologic status
Hospitals with specialized stroke teams have demonstrated significantly increased rates of
thrombolytic administration and decreased mortality. Cumulatively, the center should
identify performance measures and include mechanisms for evaluating the effectiveness of
the system as well as its component parts. The acute care of the stroke patient is more than
anything a systems-based team approach requiring the cooperation of the ED, radiology,
pharmacy, neurology, and ICU staff.
A stroke system should ensure effective interaction and collaboration among the agencies,services, and people involved in providing prevention and the timely identification, transport,
treatment, and rehabilitation of stroke patients.
For more information, seeStroke Team Creation and Primary Stroke Center Certification.
Palliative Care
Palliative care is an important component of comprehensive stroke care. Some stroke patients
will simply not recover, and others will be in a state of debilitation such that the most humane
and appropriate therapeutic concern is the comfort of the patient. Some patients have
advanced directives providing instructions for medical providers in the event of severe
medical illness or injury.Consultations
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Consultations are tailored to individual patient needs.
An experienced professional who is sufficiently familiar with stroke or a stroke team should
be available within 15 minutes of the patient's arrival in the ED. Often, occupational therapy,
physical therapy, speech therapy, and physical medicine and rehabilitation experts are
consulted within the first day of hospitalization. Consultation of cardiology and vascularsurgery or neurosurgery may be warranted based on the results of carotid duplex
scanning, neuroimaging, transthoracic and transesophageal echocardiography, and clinical
course. During hospitalization, additional useful consultations include the following:
Home health care coordinator Rehabilitation coordinator Social worker Psychiatrist (commonly for depression) Dietitian
Hemorrhagic Stroke
The terms intracerebral hemorrhage and hemorrhagic stroke are used interchangeably in this
article and are regarded as separate entities from hemorrhagic transformation of ischemicstroke. Hemorrhagic stroke is less common than ischemic stroke (ie, stroke caused by
thrombosis or embolism); epidemiologic studies indicate that only 8-18% of strokes are
hemorrhagic.[1]However, hemorrhagic stroke is associated with higher mortality rates than is
ischemic stroke. (See Epidemiology.)[2]
Patients with hemorrhagic stroke present with focal neurologic deficits similar to those of
ischemic stroke but tend to be more ill than are patients with ischemic stroke. However,
though patients with intracerebral bleeds are more likely to have headache, altered mental
status, seizures, nausea and vomiting, and/or marked hypertension, none of these findings
reliably distinguishes between hemorrhagic and ischemic stroke. (See Presentation.)[3]
Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be
obtained on an emergent basis (see the image below). Brain imaging aids in excluding
ischemic stroke, and it may identify complications of hemorrhagic stroke such as
intraventricular hemorrhage, brain edema, and hydrocephalus. Either noncontrast computed
tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the modality of
choice
Pathophysiology
In intracerebral hemorrhage, bleeding occurs directly into the brain parenchyma. The usual
mechanism is thought to be leakage from small intracerebral arteries damaged by chronic
hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation,cerebral amyloidosis, and cocaine abuse.
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Intracerebral hemorrhage has a predilection for certain sites in the brain, including the
thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by
the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass
effect of the hematoma. A general increase in intracranial pressure may occur.
Subarachnoid hemorrhageThe pathologic effects of subarachnoid hemorrhage (SAH) on the brain are multifocal. SAH
results in elevated intracranial pressure and impairs cerebral autoregulation. These effects can
occur in combination with acute vasoconstriction, microvascular platelet aggregation, and
loss of microvascular perfusion, resulting in profound reduction in blood flow and cerebral
ischemia.[4]
Etiology
The etiologies of stroke are varied, but they can be broadly categorized into ischemic or
hemorrhagic. Approximately 80-87% of strokes are from ischemic infarction caused by
thrombotic or embolic cerebrovascular occlusion. Intracerebral hemorrhages account for most
of the remainder of strokes, with a smaller number resulting from aneurysmal subarachnoidhemorrhage.[5, 6, 7, 8]
In 20-40% of patients with ischemic infarction, hemorrhagic transformation may occur within
1 week after ictus.[9, 10]
Differentiating between the different types of stroke is an essential part of the initial workup
of patients with stroke, as the subsequent management of each disorder will be vastly
different.
Risk factors
The risk of hemorrhagic stroke is increased with the following factors:
Advanced age Hypertension (up to 60% of cases) Previous history of stroke Alcohol abuse Use of illicit drugs (eg, cocaine, other sympathomimetic drugs)
Causes of hemorrhagic stroke include the following[8, 9, 11, 12, 13] :
Hypertension Cerebral amyloidosis Coagulopathies Anticoagulant therapy Thrombolytic therapy for acute myocardial infarction (MI) or acute ischemic stroke (can
cause iatrogenic hemorrhagic transformation)
Arteriovenous malformation(AVM), aneurysms, and other vascular malformations (venousand cavernous angiomas)
Vasculitis Intracranial neoplasm
Amyloidosis
Cerebral amyloidosis affects people who are elderly and may cause up to 10% of
intracerebral hemorrhages. Rarely, cerebral amyloid angiopathy can be caused by mutations
in the amyloid precursor protein and is inherited in an autosomal dominant fashion.
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Coagulopathies
Coagulopathies may be acquired or inherited. Liver disease can result in a bleeding diathesis.
Inherited disorders of coagulation such as factor VII, VIII, IX, X, and XIII deficiency can
predispose to excessive bleeding, and intracranial hemorrhage has been seen in all of these
disorders.Anticoagulant therapy
Anticoagulant therapy is especially likely to increase hemorrhage risk in patients who
metabolize warfarin inefficiently. Warfarin metabolism is influenced by polymorphism in
the CYP2C9 genes. Three known variants have been described.CYP2C9*1 is the normal
variant and is associated with typical response to dosage of warfarin. Variations *2 and *3 are
relatively common polymorphisms that reduce the efficiency of warfarin metabolism.[14]
Atrioventricular malformations
Numerous genetic causes may predispose to AVMs in the brain, although AVMs are
generally sporadic. Polymorphisms in theIL6gene increase susceptibility to a number of
disorders, including AVM. Hereditary hemorrhagic telangiectasia (HHT), previously known
as Osler-Weber-Rendu syndrome, is an autosomal dominant disorder that causes dysplasia of
the vasculature. HHT is caused by mutations inENG,ACVRL1, or SMAD4 genes. Mutations
in SMAD4 are also associated with juvenile polyposis, so this must be considered when
obtaining the patients history.
HHT is most frequently diagnosed when patients present with telangiectasias on the skin and
mucosa or with chronic epistaxis from AVMs in the nasal mucosa. Additionally, HHT can
result in AVMs in any organ system or vascular bed. AVM in the gastrointestinal tract, lungs,
and brain are the most worrisome, and their detection is the mainstay of surveillance for this
disease.
Hypertension
The most common etiology of primary hemorrhagic stroke (intracerebral hemorrhage) is
hypertension. At least two thirds of patients with primary intraparenchymal hemorrhage are
reported to have preexisting or newly diagnosed hypertension. Hypertensive small-vessel
disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in
intraparenchymal hemorrhage. Typical locations include the basal ganglia, thalami,
cerebellum, and pons.
Aneurysms and subarachnoid hemorrhageThe most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of
an intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most
frequently encountered intracranial type being the berry (saccular) aneurysm. Aneurysms
may less commonly be related to altered hemodynamics associated with AVMs, collagen
vascular disease, polycystic kidney disease, septic emboli, and neoplasms.
Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen. This
phenomenon is thought to arise from capillary or venous rupture. It has a less severe clinical
course and, in general, a better prognosis.
Berry aneurysms are most often isolated lesions whose formation results from a combination
of hemodynamic stresses and acquired or congenital weakness in the vessel wall. Saccular
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aneurysms typically occur at vascular bifurcations, with more than 90% occurring in the
anterior circulation. Common sites include the following:
The junction of the anterior communicating arteries and anterior cerebral arteriesmostcommonly, the middle cerebral artery (MCA) bifurcation
The supraclinoid internal carotid artery at the origin of the posterior communicating artery
The bifurcation of the internal carotid artery (ICA)Genetic causes of aneurysms
Intracranial aneurysms may result from genetic disorders. Although rare, several families
have been described that have a predispositioninherited in an autosomal dominant
fashionto intracranial berry aneurysms. A number of genes, all categorized asANIB genes,
are associated with this predisposition. Presently,ANIB1 throughANIB11 are known.
Autosomal dominant polycystic kidney disease (ADPKD) is another cause of intracranial
aneurysm. Families with ADPKD tend to show phenotypic similarity with regard to
intracranial hemorrhage or asymptomatic berry aneurysms.[15]
Loeys-Dietz syndrome (LDS) consists of craniofacial abnormalities, craniosynostosis,
marked arterial tortuosity, and aneurysms and is inherited in an autosomal dominant manner.
Although intracranial aneurysms occur in LDS of all types, saccular intracranial aneurysms
are a prominent feature of LDS type IC, which is caused by mutations in the SMAD3 gene.[16]
Ehlers-Danlos syndrome is a group of inherited disorders of the connective tissue that feature
hyperextensibility of the joints and changes to the skin, including poor wound healing,
fragility, and hyperextensibility. However, Ehlers-Danlos vascular type (type IV) also is
known to cause spontaneous rupture of hollow viscera and large arteries, including arteries in
the intracranial circulation.
Patients with Ehlers-Danlos syndrome may also have mild facial findings, including lobeless
ears, a thin upper lip, and a thin, sharp nose. The distal fingers may appear prematurely aged
(acrogeria). In the absence of a suggestive family history, it is difficult to separate Ehlers-
Danlos vascular type from other forms of Ehlers-Danlos. Ehlers-Danlos vascular type is
caused by mutations in the COL3A1 gene; it is inherited in an autosomal dominant manner.
Hemorrhagic transformation of ischemic stroke
Hemorrhagic transformation represents the conversion of a bland infarction into an area of
hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of
ischemically injured tissue, either from recanalization of an occluded vessel or from collateral
blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruptionof the blood-brain barrier, red blood cells extravasate from the weakened capillary bed,
producing petechial hemorrhage or frank intraparenchymal hematoma.[8, 9, 17] (For more
information, seeReperfusion Injury in Stroke.)
Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days postictus, usually
within the first week. It is more commonly seen following cardioembolic strokes and is more
likely with larger infarct size.[8, 10, 18]Hemorrhagic transformation is also more likely
following administration of tissue plasminogen activator (tPA) in patients whose noncontrast
computed tomography (CT) scans demonstrate areas of hypodensity.
Prognosis
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The prognosis in patients with hemorrhagic stroke varies depending on the severity of stroke
and the location and the size of the hemorrhage. Lower Glasgow Coma Scale (GCS) scores
are associated with poorer prognosis and higher mortality rates. A larger volume of blood at
presentation is also associated with a poorer prognosis. Growth of the hematoma volume is
associated with a poorer functional outcome and increased mortality rate.
The intracerebral hemorrhage score is the most commonly used instrument for predicting
outcome in hemorrhagic stroke. The score is calculated as follows:
GCS score 3-4: 2 points GCS score 5-12: 1 point GCS score 13-15: 0 points Age 80 years: Yes, 1 point; no, 0 points Infratentorial origin: Yes, 1 point; no, 0 points Intracerebral hemorrhage volume 30 cm3: 1 point Intracerebral hemorrhage volume < 30 cm3: 0 points Intraventricular hemorrhage: Yes, 1 point; no, 0 points
In a study by Hemphill et al, all patients with an Intracerebral Hemorrhage Score of 0
survived, and all of those with a score of 5 died; 30-day mortality increased steadily with the
Score.[27]
Other prognostic factors include the following:
Nonaneurysmal perimesencephalic stroke has a less severe clinical course and, in general, abetter prognosis
The presence of blood in the ventricles is associated with a higher mortality rate; in onestudy, the presence of intraventricular blood at presentation was associated with a mortality
increase of more than 2-fold
Patients with oral anticoagulation-associated intracerebral hemorrhage have highermortality rates and poorer functional outcomes
In studies, withdrawal of medical support or issuance of Do Not Resuscitate (DNR) orders
within the first day of hospitalization predict poor outcome independent of clinical factors.
Because limiting care may adversely impact outcome, American Heart Association/American
Stroke Association (AHA/ASA) guidelines suggest that new DNR orders should probably be
postponed until at least the second full day of hospitalization. Patients with DNRs should be
given all other medical and surgical treatment, unless the DNR explicitly says otherwise.
History
Obtaining an adequate history includes determining the onset and progression of symptoms,
as well as assessing for risk factors and possible causative events. Such risk factors includethe following:
Previous transient ischemic attack (TIA) and stroke Hypertension Diabetes Smoking Arrhythmia and valvular disease Illicit drug use Use of anticoagulants Risk factors for thrombosis
A history of trauma, even if minor, may be important, as extracranial arterial dissections canresult in ischemic stroke.
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Hemorrhagic versus ischemic stroke
Symptoms alone are not specific enough to distinguish ischemic from hemorrhagic stroke.
However, generalized symptoms, including nausea, vomiting, and headache, as well as an
altered level of consciousness, may indicate increased intracranial pressure and are more
common with hemorrhagic strokes and large ischemic strokes.
Seizures are more common in hemorrhagic stroke than in the ischemic kind. Seizures occur
in up to 28% of hemorrhagic strokes, generally at the onset of the intracerebral hemorrhage or
within the first 24 hours.
Focal neurologic deficits
The neurologic deficits reflect the area of the brain typically involved, and stroke syndromes
for specific vascular lesions have been described. Focal symptoms of stroke include the
following:
Weakness or paresis that may affect a single extremity, one half of the body, or all 4extremities
Facial droop Monocular or binocular blindness Blurred vision or visual field deficits Dysarthria and trouble understanding speech Vertigo or ataxia Aphasia
Subarachnoid hemorrhage
Symptoms of subarachnoid hemorrhage may include the following:
Sudden onset of severe headache Signs of meningismus with nuchal rigidity Photophobia and pain with eye movements Nausea and vomiting Syncope - Prolonged or atypical
The most common clinical scoring systems for grading aneurysmal subarachnoid hemorrhage
are the Hunt and Hess grading scheme and the World Federation of Neurosurgeons (WFNS)
grading scheme, which incorporates the Glasgow Coma Scale. The Fisher Scale incorporates
findings from noncontrast computed tomography (NCCT) scans.
Physical Examination
The assessment in patients with possible hemorrhagic stroke includes vital signs; a generalphysical examination that focuses on the head, heart, lungs, abdomen, and extremities; and a
thorough but expeditious neurologic examination.[28]However, intracerebral hemorrhage may
be clinically indistinguishable from ischemic stroke. (Though stroke is less common in
children, the clinical presentation is similar.)
Hypertension (particularly systolic blood pressure [BP] greater than 220 mm Hg) is
commonly a prominent finding in hemorrhagic stroke. Higher initial BP is associated with
early neurologic deterioration, as is fever.[28]
An acute onset of neurologic deficit, altered level of consciousness/mental status, or coma is
more common with hemorrhagic stroke than with ischemic stroke. Often, this is caused by
increased intracranial pressure. Meningismus may result from blood in the subarachnoidspace.
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Examination results can be quantified using various scoring systems. These include the
Glasgow Coma Scale (GCS), the Intracerebral Hemorrhage Score (which incorporates the
GCS; see Prognosis), and theNational Institutes of Health Stroke Scale.
Focal neurologic deficits
The type of deficit depends upon the area of brain involved. If the dominant hemisphere(usually the left) is involved, a syndrome consisting of the following may result:
Right hemiparesis Right hemisensory loss Left gaze preference Right visual field cut Aphasia Neglect (atypical)
If the nondominant (usually the right) hemisphere is involved, a syndrome consisting of the
following may result:
Left hemiparesis Left hemisensory loss Right gaze preference Left visual field cut
Nondominant hemisphere syndrome may also result in neglect when the patient has left-sided
hemi-inattention and ignores the left side.
If the cerebellum is involved, the patient is at high risk for herniation and brainstem
compression. Herniation may cause a rapid decrease in the level of consciousness and may
result in apnea or death.
Specific brain sites and associated deficits involved in hemorrhagic stroke include thefollowing:
Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gazeparesis, homonymous hemianopia, aphasia, neglect, or apraxia
Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymoushemianopia, miosis, aphasia, or confusion
Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis,homonymous hemianopia, abulia, aphasia, neglect, or apraxia
Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, orconfusion
Brainstem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis,ocular bobbing, miosis, or autonomic instability
CerebellumIpsilateral ataxia, facial weakness, sensory loss; gaze paresis, skew deviation,miosis, or decreased level of consciousness
Other signs of cerebellar or brainstem involvement include the following:
Gait or limb ataxia Vertigo or tinnitus Nausea and vomiting Hemiparesis or quadriparesis Hemisensory loss or sensory loss of all 4 limbs Eye movement abnormalities resulting in diplopia or nystagmus Oropharyngeal weakness or dysphagia
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Crossed signs (ipsilateral face and contralateral body)Many other stroke syndromes are associated with intracerebral hemorrhage, ranging from
mild headache to neurologic devastation. At times, a cerebral hemorrhage may present as a
new-onset seizure.
TreatmentThe treatment and management of patients with acute intracerebral hemorrhage depends on
the cause and severity of the bleeding. Basic life support, as well as control of bleeding,
seizures, blood pressure (BP), and intracranial pressure, are critical. Medications used in the
treatment of acute stroke include the following:
Anticonvulsants - To prevent seizure recurrence Antihypertensive agents - To reduce BP and other risk factors of heart disease Osmotic diuretics - To decrease intracranial pressure in the subarachnoid space
Management begins with stabilization of vital signs. Perform endotracheal intubation for
patients with a decreased level of consciousness and poor airway protection. Intubate and
hyperventilate if intracranial pressure is elevated, and initiate administration of mannitol forfurther control. Rapidly stabilize vital signs, and simultaneously acquire an emergent
computed tomography (CT) scan. Glucose levels should be monitored, with normoglycemia
recommended.[28]Antacids are used to prevent associated gastric ulcers.
Currently, no effective targeted therapy for hemorrhagic stroke exists. Studies of recombinant
factor VIIa (rFVIIa) have yielded disappointing results. Evacuation of hematoma, either via
open craniotomy or endoscopy, may be a promising ultra-early-stage treatment for
intracerebral hemorrhage that may improve long-term prognosis.
Management of Seizures
Early seizure activity occurs in 4-28% of patients with intracerebral hemorrhage; theseseizures are often nonconvulsive.[30, 31] According to American Heart Association/American
Stroke Association (AHA/ASA) 2010 guidelines for the management of spontaneous
intracerebral hemorrhage, patients with clinical seizures or electroencephalographic (EEG)
seizure activity accompanied by a change in mental status should be treated with antiepileptic
drugs.[28]
Patients for whom treatment is indicated should immediately receive a benzodiazepine, such
as lorazepam or diazepam, for rapid seizure control. This should be accompanied by
phenytoin or fosphenytoin loading for longer-term control.
Prophylaxis
The utility of prophylactic anticonvulsant medication remains uncertain. In prospective and
population-based studies, clinical seizures have not been associated with worse neurologic
outcome or mortality. Indeed, 2 studies have reported worse outcomes in patients who did not
have a documented seizure but who received antiepileptic drugs (primarily phenytoin).[28]
The 2010 AHA/ASA guidelines do not offer recommendations on prophylactic
anticonvulsants, but suggest that continuous EEG monitoring is probably indicated in patients
with intracranial hemorrhage whose mental status is depressed out of proportion to the degree
of brain injury
Prophylactic anticonvulsant therapy has been recommended in patients with lobar
hemorrhages to reduce the risk of early seizures. One large, single-center study showed that
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prophylactic antiepileptic drugs significantly reduced the number of clinical seizures in these
patients.[30]
In addition, AHA/ASA guidelines from 2012 suggest that prophylactic anticonvulsants may
be considered for patients with aneurysmal subarachnoid hemorrhage. In such cases,
however, anticonvulsant u