11/02/2022
New Stroke Risk Score Developed for COVID PatientsResearchers have developed a quick and easy scoring system to predict which hospitalized COVID-19 patients are more at risk for stroke.
Dr Alexander Merkler
The system is simple. You can calculate the points in 5 seconds, and then predict the chances the patient will have a stroke Alexander E. Merkler, MD, assistant professor of neurology at Weill Cornell Medical College/NewYork- Presbyterian Hospital in New York City, and lead author of a study of the system, told theheart The new system will allow clinicians to stratify patients and lead to closer monitoring of those at highest risk for stroke, said Merkler.
The study was presented during the 2022 International Stroke Conference (ISC) being held in New Orleans this week.
Some, but not all, studies suggest COVID-19 increases the risk of stroke and worsens stroke outcomes, and the association isn't clear, investigators note.
Researchers used the American Heart Association (AHA) Get With the Guidelines COVID-19 cardiovascular disease registry for this analysis. They evaluated 21,420 adult patients (mean age 61 years, 54% men), who were hospitalized with COVID-19 at 122 centers from March 2020 to March 2021.
Investigators tapped into the vast amounts of data in this registry on different variables including demographics, comorbidities, and lab values.
The outcome was a cerebrovascular event, defined as any ischemic or hemorrhagic stroke, transient ischemic attack (TIA), or cerebral vein thrombosis. Of the total hospitalized COVID-19 population, 312 (1.5%) had a cerebrovascular event.
Researchers first used standard statistical models to determine which risk factors are most associated with the development of stroke. They identified six such factors:history of stroke
no fever at the time of hospital admission
no history of pulmonary disease
high white blood cell count
history of hypertension
high systolic blood pressure at the time of hospital admission
That the list of risk factors included absence of fever and history of pulmonary disease was somewhat surprising, said Merkler, but there may be possible explanations, he added.
A high fever is an inflammatory response and perhaps patients who aren't responding appropriately "could be sicker in general and have a poor immune system, and thereby be at increased risk for stroke," said Merkler.
In the case of pulmonary disease, patients without a history who are admitted for COVID "may have an extremely high burden of COVID, or are extremely sick, and that's why they're at higher risk for stroke."
The scoring system assigns points for each variable, with more points conferring a higher risk of stroke. For example, someone who has 0-1 points has 0.2% risk of having a stroke but someone with 4-6 points has 2% to 3% risk, said Merkler.
"So, we're talking about a 10- to 15-fold increased risk of having a stroke with 4 to 6 vs 0 to 1 variables."
The accuracy of the risk stratification score (C-statistic of 0.66; 95% CI, 0.60 - 0.72) is "fairly good or modestly good," said Merkler.
A patient with a score of 5 or 6 may need more vigilant monitoring to make sure symptoms are caught early and therapies such as thrombolytics and thrombectomy are readily available, he added.
Researchers also used a sophisticated machine-learning approach where a computer takes all the variables and identifies the best algorithm to predict stroke.
"The machine-learning algorithm was basically just as good as our standard model; it was almost identical," said Merkler.
Outside of COVID, other scoring systems are used to predict stroke. For example, the ABCD2 score uses various factors to predict risk of recurrent stroke.
Commenting on the study for theheart.org | Medscape Cardiology, Philip B. Gorelick, MD, adjunct professor, Northwestern University Feinberg School of Medicine, Chicago, Illinois, said the results are promising, as they may lead to identifying modifiable factors to prevent stroke.
Gorelick noted the authors identified risk factors to predict risk of stroke "after an extensive analysis of baseline factors that included an internal validation process."
The finding that no fever and no history of pulmonary disease were included in those risk factors was "unexpected," said Gorelick, who is also medical director of the Hauenstein Neuroscience Center in Grand Rapids, Michigan. "This may reflect the baseline timing of data collection."
He added further validation of the results in other data sets "will be useful to determine the consistency of the predictive model and its potential value in general practice."Louise D. McCullough, MD, PhD, professor and chair of neurology, McGovern Medical School, The University of Texas Health Science Center, Houston, said the association between stroke risk and COVID exposure "has been very unclear."
"Some people find a very strong association between stroke and COVID, some do not," said McCullough, who served as the chair of the ISC 2022 meeting.
This new study looking at a risk stratification model for COVID patients was "very nicely done," she added.
"They used the American Heart Association Get With The Guidelines COVID registry, which was an amazing feat that was done very quickly by the AHA to establish COVID reporting in the Get With The Guidelines data, allowing us to really look at other factors related to stroke that are in this unique database."
The study received funding support from the American Stroke Association. Merkler has received funding from the American Heart Association and the Leon Levy Foundation. Gorelick was not involved in the study and has disclosed no relevant financial relationships Practice Essentials
Ischemic stroke (see the image below) is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke. Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic stroke. SECTIONS Practice Essentials
Ischemic stroke (see the image below) is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery and is more common than hemorrhagic stroke.
Maximum intensity projection (MIP) image from a co
Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.
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See Acute Stroke, a Critical Images slideshow, for more information on incidence, presentation, intervention, and additional resources.
Signs and symptoms
Consider stroke in any patient presenting with acute neurologic deficit or any alteration in level of consciousness. Common stroke signs and symptoms include the following:
Abrupt onset of hemiparesis, monoparesis, or (rarely) quadriparesis
Hemisensory deficits
Monocular or binocular visual loss
Visual field deficits
Diplopia
Dysarthria
Facial droop
Ataxia
Vertigo (rarely in isolation)
Nystagmus
Aphasia
Sudden decrease in level of consciousness
Although such symptoms can occur alone, they are more likely to occur in combination. No historical feature distinguishes ischemic from hemorrhagic stroke, although nausea, vomiting, headache, and sudden change in level of consciousness are more common in hemorrhagic strokes. In younger patients, a history of recent trauma, coagulopathies, illicit drug use (especially co***ne), migraines, or use of oral contraceptives should be elicited.
With the availability of reperfusion options (fibrinolytic and endovascular therapies) 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 stroke symptoms (neurologic deficits)
Distinguishing stroke from stroke mimics
Establishing a neurologic baseline, should the patient's condition improve or deteriorate
Establishing stroke severity, using a structured neurologic exam and score (National Institutes of Health Stroke Scale [NIHSS]) to assist in prognosis and therapeutic selection
Essential components of the neurologic examination include the following evaluations:
Cranial nerves
Motor function
Sensory function
Cerebellar function
Gait
Deep tendon reflexes
Language (expressive and receptive capabilities)
Mental status and level of consciousness
The skull and spine also should be examined, and signs of meningismus should be sought.
See Clinical Presentation for more detail.
Diagnosis
Emergent brain imaging is essential for evaluation of acute ischemic stroke. Noncontrast computed tomography (CT) scanning is the most commonly used form of neuroimaging in the acute evaluation of patients with apparent acute stroke. The following neuroimaging techniques may also be used emergently:
CT angiography and CT perfusion scanning
Magnetic resonance imaging (MRI)
Carotid duplex scanning
Digital subtraction angiography
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
Laboratory studies
Laboratory tests performed in the diagnosis and evaluation of ischemic stroke include the following:
Complete blood count (CBC): A baseline study that may reveal a cause for the stroke (eg, polycythemia, thrombocytosis, leukemia), provide evidence of concurrent illness, and ensure absence of thrombocytopenia when considering fibrinolytic therapy
Basic chemistry panel: A baseline study that may reveal a stroke mimic (eg, hypoglycemia, hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency)
Coagulation studies: May reveal a coagulopathy and are useful when fibrinolytics or anticoagulants are to be used
Cardiac biomarkers: Important because of the association of cerebral vascular disease and coronary artery disease
Toxicology screening: May assist in identifying intoxicated patients with symptoms/behavior mimicking stroke syndromes or the use of sympathomimetics, which can cause hemorrhagic and ischemic strokes
Pregnancy testing: A urine pregnancy test should be obtained for all women of childbearing age with stroke symptoms; recombinant tissue-type plasminogen activator (rt-PA) is a pregnancy class C agent
See Workup for more detail.
Management
The goal for the emergent management of stroke is to complete the following within 60 minutes or less of patient arrival: [1]
Assess airway, breathing, and circulation (ABCs) and stabilize the patient as necessary
Complete the initial evaluation and assessment, including imaging and laboratory studies
Initiate reperfusion therapy, if appropriate
Critical treatment decisions focus on the following:
The need for airway management
Optimal blood pressure control
Identifying potential reperfusion therapies (eg, intravenous fibrinolysis with rt-PA (alteplase) or intra-arterial approaches)
Involvement of a physician with a special interest and training in stroke is ideal. Stroke care units with specially trained nursing and allied healthcare personnel have clearly been shown to improve outcomes.
Ischemic stroke therapies include the following:
Fibrinolytic therapy
Antiplatelet agents [2, 3]
Mechanical thrombectomy
Treatment of comorbid conditions may include the following:
Reduce fever
Correct hypotension/significant hypertension
Correct hypoxia
Correct hypoglycemia
Manage cardiac arrhythmias
Manage myocardial ischemia
Stroke prevention
Primary stroke prevention refers to the treatment of individuals with no previous history of stroke. Measures may include use of the following:
Platelet antiaggregants
Statins
Exercise
Lifestyle interventions (eg, smoking cessation, alcohol moderation)
Secondary prevention refers to the treatment of individuals who have already had a stroke. Measures may include use of the following:
Platelet antiaggregants
Antihypertensives
Statins
Lifestyle interventions
See Treatment and Medication for more detail.
Background
Acute ischemic stroke (AIS) is characterized by the sudden loss of blood circulation to an area of the brain, typically in a vascular territory, resulting in a corresponding loss of neurologic function. Also previously called cerebrovascular accident (CVA) or stroke syndrome, stroke is a nonspecific state of brain injury with neuronal dysfunction that has several pathophysiologic causes. Strokes can be divided into 2 types: hemorrhagic or ischemic. Acute ischemic stroke is caused by thrombotic or embolic occlusion of a cerebral artery. (See the image below.)
Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.
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Nearly 800,000 people suffer strokes each year in the United States; 82–92% of these strokes are ischemic. Stroke is the fifth leading cause of adult death and disability, resulting in over $72 billion in annual cost. [4] Between 2012 and 2030, total direct medical stroke-related costs are projected to triple, to $184.1 billion, with the majority of the projected increase in costs arising from those 65 to 79 years of age. [5]
Ischemic and hemorrhagic stroke cannot be reliably differentiated on the basis of clinical examination findings alone. Further evaluation, especially with brain imaging tests (ie, computed tomography [CT] scanning or magnetic resonance imaging [MRI]), is required. (See Workup.)
Stroke categories
The system of categorizing stroke developed in the multicenter Trial of ORG 10172 in Acute Stroke Treatment (TOAST) divides ischemic strokes into the following 3 major subtypes: [2]
Large-artery
Small-vessel, or lacunar
Cardioembolic infarction
Large-artery infarctions often involve thrombotic in situ occlusions on atherosclerotic lesions in the carotid, vertebrobasilar, and cerebral arteries, typically proximal to major branches; however, large-artery infarctions may also be cardioembolic.
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. [6] (See Pathophysiology.)
Small vessel or lacunar strokes are associated with small focal areas of ischemia due to obstruction of single small vessels, typically in deep penetrating arteries, that generate a specific vascular pathology.
In many patients the exact etiology of their stroke is not identified and these are classified as cryptogenic strokes.
Treatment
Recanalization strategies, including intravenous recombinant tissue-type plasminogen activator (alteplase or rt-PA) and intra-arterial approaches, attempt to establish revascularization so that cells within the ischemic penumbra (a metabolically active region, peripheral to the ischemic area, where blood flow is reduced and the cells are potentially viable) can be rescued before irreversible injury occurs. Restoring blood flow can mitigate the effects of ischemia only if performed quickly.
The US Food and Drug Administration (FDA) has approved the use of rt-PA in patients who meet criteria set forth by the National Institute of Neurologic Disorders and Stroke (NINDS). In particular, rt-PA must be given within 3 hours of stroke onset and only after CT scanning has ruled out hemorrhagic stroke.
On the basis of recent European data, the American Heart Association and American Stroke Association recommended expanding the window of treatment from 3 hours to 4.5 hours, with more stringent exclusion criteria for the later period (see Treatment). The FDA has not approved rt-PA for this expanded indication, but this has become the community standard in many institutions.
Other aspects of treatment for acute ischemic stroke include the following:
Optimization of physiologic parameters and prevention of neurologic complications
Supplemental oxygen as required (> 94% SaO2)
Glycemic control
Optimal blood pressure control (with consideration for reperfusion therapies)
Prevention of hyperthermia
See also Hemorrhagic Stroke.
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.
Knowledge of cerebrovascular arterial anatomy and the territories supplied by the cerebral arteries is useful in determining which vessels are involved in acute stroke. Atypical patterns of brain ischemia that do not conform to specific vascular distributions may indicate a diagnosis other than ischemic stroke, such as venous infarctionArterial distributions
In a simplified model, 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. (See the image below.)
Lateral view of a cerebral angiogram illustrates t
Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery (MCA), with the apex representing the Sylvian point.
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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 MCA is the dominant source of vascular supply to the hemispheres. (See the images below.)
The supratentorial vascular territories of the maj
The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (MCA; red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes; insula; and basal ganglia. The anterior cerebral artery (ACA; blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (PCA; green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
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Frontal view of a cerebral angiogram with selectiv
Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery (ICA) illustrates the anterior circulation. The anterior cerebral artery (ACA) consists of the A1 segment proximal to the anterior communicating artery, with the A2 segment distal to it. The middle cerebral artery (MCA) can be divided into 4 segments: the M1 (horizontal segment) extends to the anterior basal portion of the insular cortex (the limen insulae) and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).
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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. (See Table 1, below.)
The cerebellar hemispheres are supplied as follows:
Inferiorly by the posterior inferior cerebellar artery (PICA), arising from the vertebral artery (see the image below)
Frontal projection from a right vertebral artery a
Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICAs) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICAs) arise from the proximal basilar artery. The superior cerebellar arteries (SCAs) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries (PCAs).
