Stroke is the fourth leading cause of death1 and one of the leading conditions that cause major functional disability in the United States. In 2010, medical care for stroke victims cost approximately $54 billion and is expected to reach over $1 trillion by 2050. Each year, approximately 800,000 individuals suffer a stroke with an average of one stroke every 40 seconds.2,3 Although stroke can occur at any age, the incidence of stroke increases with advancing age. While the frequency of stroke is higher among males than females, older females suffer strokes more frequently than older males. Blacks have twice the risk of stroke in comparison with Whites.4 Inactivity, obesity, and hypertension lead the risk factors predisposing individuals to stroke.5
Classification of stroke
The two main classifications of stroke are ischemic stroke and hemorrhagic stroke. Approximately 87% of strokes are ischemic, 10% are hemorrhagic, and 3% are caused by subarachnoid hemorrhage.1 Ischemic strokes are the result of an interruption in cerebral blood flow causing necrosis to brain tissue; some examples of this stroke are stenosis, thrombus, or thromboemboli. Hemorrhagic strokes, however, result from leakage or bleeding into the brain vault caused by hypertension, aneurysm, arteriovenous malformation (AVM), head injury, or blood dyscrasias. Each stroke type results with interruption in cerebral perfusion, and while risk factors for both can differ, many are similar.6,7
Risk factors for stroke include hypertension, inactivity, obesity, alcohol consumption, increased cholesterol, bleeding disorders, diabetes, and heredity. Race, gender, and age are also risk factors for stroke, as well as illicit drug use and smoking. According to the American Heart Association, patients with blood pressures less than 120/80 have half the lifetime risk of developing a stroke than those with hypertension.2 Heart diseases, specifically in those predisposed to clot formation, can lead to cardioembolic stroke. In addition, bleeding disorders can affect clot development in the cerebral vessels leading to hypoperfusion and possible emboli.7
Alcohol can lead to a stroke in multiple ways; it can cause cardiac dysrhythmias—creating emboli—which can lead to cerebral embolism. People who use illicit drugs such as cocaine are at greater risk for stroke because the drug induces vasospasm, increases heart rate, BP, and metabolic rate. Smoking releases many toxins into the systemic circulation, which damages the lining of the vessels in the circulatory system, leading to atherosclerosis. Smoking also narrows or blocks the blood vessels leading to platelet aggregation, which in turn increases the chances of developing a blood clot. Overweight and obese individuals have an increased risk of stroke secondary to the association of obesity with a high-fat diet, higher BPs, and decreased exercise.7–11
A significant precursor to stroke is a reversible episode of focal neurologic deficits or transient ischemic attack (TIA). Typically, symptoms of a TIA last seconds to minutes, and rarely last up to 12 hours. Patients diagnosed with TIA are at significantly greater risk to have major stroke. In fact, 10% to 20% of individuals with TIA will have a stroke within 90 days of its diagnosis.12,13
Overview of pathophysiology
Stroke—an interruption of the blood flow to the brain—initiates a process of metabolic actions referred to as the ischemic cascade. Interruption of blood flow can be due to a number of causes such as emboli, thrombus, general hypoperfusion from systemic disease, or an accumulation of blood in the skeletal vault—all of which will affect the normal cerebral perfusion rate. Normal cerebral blood flow is 750 mL/minute; once the blood flow decreases below 25 mL/minute, the ischemic cascade is initiated. At this low level of perfusion, neurons cannot adequately maintain aerobic respiration and required nutrients, so the cells must then convert to anaerobic respiration. This type of respiration produces by-products of lactic acid that alter the pH level, causing ineffective anaerobic respiration. This leaves neurons without the ability to produce a satisfactory volume of adenosine triphosphate (ATP) to replenish depolarization. Altered levels of ATP disrupt the homeostasis of the cells and result in electrolyte disturbances, which cause sodium and potassium to enter the cell, and increase calcium accumulation. The newly injured ischemic cells produce glutamate, which damages neurons even further. In addition, faulty homeostasis causes an increase in water entering the cell causing cell rupture, injury, death, and destruction of adjacent neurons.14,15
As an ischemic stroke is evolving, a central area of dead or dying tissue exists around the vicinity of infarction known as the penumbra region. This is an area of minimally perfused cells with impaired metabolic functions. Calcium and glutamate continue to enter the cell resulting in additional free radical production and vasoconstriction, which damages neuron pathways, possibly expanding the area of infarction and extending the stroke. Survival of the cells in the penumbra depends on the well-timed return of cerebral blood flow, the amount of toxins produced by adjacent cells, cerebral edema, and altered blood flow. It is possible that ischemic but viable tissue can be saved.16
Clinical manifestations of stroke
Clinical presentations of ischemic stroke are based on the cerebral vessel affected, the area of the brain supplied by the vessel, and the degree of collateral circulation. Stroke is usually associated with sudden rapid onset in addition to focal unilateral symptoms. The most common symptoms of ischemic stroke include facial hemiparesis and upper/lower extremity paresis or paralysis. Symptoms can also be unilateral—with possible hemianopia, aphasia, dysarthria—or sudden, unexplained ataxia.17
Hemorrhagic stroke–clinical signs and symptoms
While the focus of this article is on ischemic stroke, it is important to understand the presentation of hemorrhagic stroke as well (see Hemorrhagic stroke). This type of stroke includes focal neurologic symptoms, headache, neck pain or rigidity, nausea, vomiting, decreased level of consciousness, visual disturbances such as light sensitivity, diplopia, or ptosis.18 Common types of hemorrhagic stroke include intracerebral hemorrhage, intracranial aneurysm, AVMs, and subarchnoid hemorrhage. The patient with hemorrhagic stroke usually reports a severe headache; the most common symptoms include vomiting, sudden loss of consciousness, and focal seizures. Patients with AVM complain of nuchal rigidity, spinal pain, diplopia, ptosis, tinnitus, and dizziness.Hemiparesis may also occur.19 People between the ages 45 and 64 suffering a hemorrhagic stroke have approximately a 38% chance of death within 30 days. Hemorrhagic stroke can sometimes be treated surgically to repair an aneurysm or evacuate a blood clot.2
Ischemic stroke–clinical signs and symptoms
Signs of ischemic stroke are based on its location (see Cerebral arteries). These strokes can occur in the middle cerebral artery and present with both left and right middle cerebral artery syndrome. Other presentations include anterior cerebral artery, posterior cerebral artery, and vertebrobasilar artery. The general clinical presentation of ischemic stroke includes hemiparesis or hemiplegia, acute sensory loss, complete or partial hemianopia, visual field deficits, dysarthria, aphasia, ataxia, vertigo, nystagmus, and sudden decrease or loss of consciousness; signs and symptoms may differ based on vessels involved.18
Middle cerebral artery complete stroke presents with contralateral hemiparesis, contralateral hemianesthesia hypestheia, hemianopsia (with eye gaze preference toward the side of the lesion), agnosia, and receptive or expressive aphasia; if the lesion is in the dominant hemisphere, neglect/inattention or extinction in nondominant hemisphere lesion present.18,20
Left middle cerebral artery syndrome presents with language loss, right hemiparesis, hemianesthesia, a cut right visual field, and left gaze preference.21,22
Right middle cerebral artery syndrome presents with left hemineglect (both visual and spatial), left hemiparesis, left hemisensory loss (with left visual field cut), and anasgosia.20
Anterior cerebral artery stroke clinical manifestations include possible primitive reflexes such as grasping and sucking. Cognitive changes include altered mental status and impaired judgment. In addition, other characteristics are speech preservation, contralateral weakness of the lower extremities, contralateral cortical sensory deficits, gait apraxia, and urinary incontinence.18,22
Clinical manifestations of posterior cerebral artery stroke include visual changes such as cortical blindness, visual agnosia, and disorders of color vision. Other manifestations include memory impairment, altered mental status, and temporary amnesia.18,23
Vertebrobasilar artery syndrome stroke's clinical signs and symptoms are related to various cranial nerves depending on the location of the infarct in the artery (usually cranial nerves 3, 6, 7, or 11), as well as cerebellar and brainstem deficits. Clinical manifestations include alterations in mental status, asymmetrical hemi or quadraparesis, vertigo, nystagmus, diplopia, dysphagia, dysarthria, focal hypesthesia, syncope, and ataxia.18,24
Stroke management and treatment
The goals during acute stroke are to stabilize the patient, reduce mortality, limit infarct size, prevent complications, and reduce the potential of long-term disability. Critical steps are needed to evaluate the underlying cause of the stroke and identification of any causative comorbidities contributing to the event; requiring interventions as these comorbidities can impact stroke recovery. In order to effectively meet these goals, it is essential that treatment and necessary interventions begin within 1 hour of the patient's arrival or onset of symptoms. The completion of history, physical exam, current medications, lab studies, and diagnostic imaging are included in the workup.25,26
Initial assessment and management includes:
- Airway and oxygen
- - N.P.O. –aspiration/dysphagia precautions while awaiting swallowing evaluation.
- - Monitor oxygen saturation levels and administer oxygen if the oxygen saturation falls below 95%; head of the bed elevated 30 degrees to increase oxygenation and for patients at risk for increased intracranial pressure.
- - Endotracheal tube intubation p.r.n.–intubation may be required if hypoxic and/or hypercapnic.
- I.V. access for patients who are candidates for fibrinolytic therapy
- Vital signs–BP—should be maintained below 185/110 for patients who may be eligible for fibrinolytic therapy. Heart rate should be monitored to assess cardiac rhythm irregularities, which may produce an embolic event. Respiratory assessment (as stroke can decrease the respiratory drive); assessment of respiratory comorbidities is essential. Temperature evaluation is critical as an elevated temperature can expand ischemic injury.
- Blood glucose levels—elevated glucose levels can increase ischemic injury and decrease penumbra recovery; decreased blood glucose levels or hypoglycemia can produce similar symptoms as stroke.
- Evaluation of nausea, vomiting (common in hemorrhagic stroke), and rule out neck rigidity.
- It is recommended to complete the National Institutes of Health Stroke Scale (NIHSS). The NIHSS uses a 42-point scale based on neurologic deficits such as consciousness, sensation, speech, movement, and language, to reflect the patient's neurologic status. A score of 42 is indicative of a severe stroke; the stroke scale can be helpful when considering treatment with fibrinolytic therapy.27
- The neurologic assessment to include the most crucial point and the time of onset of stroke. Additionally, the course of stroke with history and type of symptoms, level of consciousness using the Glasgow Coma Scale, paresis of extremities, sensory deficits, coordination, dysphasia, hemianopia, or loss of cortical functioning. The neurologic history should include prior history of subdural hematoma, intracranial hemorrhage, TIAs, or carotid stenosis.25–31
Other diagnostic evaluations
Additional lab evaluations include blood chemistries, a complete blood count with platelets, prothrombin time/international normalized ratio (PT/INR), and partial thromboplastin time—for patients taking warfarin, heparin, other anticoagulants, or for those with liver dysfunction. Coagulation studies are important prior to the treatment of ischemic stroke in order to assess the potential risk of hemorrhage if patients are candidates for fibrinolytic therapy. Other essential lab tests include a lipid profile, toxicology screen, blood alcohol levels, and pregnancy testing (if the patient is of childbearing age). In patients where an intracerebral bleed is suspected, a type and cross match may be necessary.28,31,32
Focused physical exam
A brief but focused physical exam includes an evaluation of trauma that may have caused the stroke—hemorrhagic strokes present with a severe headache. Patients who have had seizures can have tongue lacerations or contusions. In addition, intracranial vascular lesions present with retro-orbital bruits. Patients with increased intracranial pressure will have papilledema, while those with arteriosclerotic heart disease may have carotid bruits. A patient with heart failure will present with jugular venous distention. Expanded cardiac assessment for atrial fibrillation, myocardial infarction, and murmurs can indicate cardiogenic causes of stroke. Peripheral vascular assessment of pulses can indicate atherosclerotic heart disease. A skin assessment is necessary to evaluate for indicators of coagulopathies such as jaundice, ecchymosis, purpura, and petechiae.26,28,32
Diagnostic neuroimaging is essential to establish the cause of stroke, and vessel pathology is recommended prior to initiating any therapy. Current practice guidelines indicate that patients should have a computed tomography (CT) scan within 24 hours.28,33 Imaging studies can differentiate the disruption of blood flow and identify entities that can mimic stroke such as tumors. Magnetic resonance imaging (MRI) can be used to supplement the CT scan. In addition, hemodynamic and vascular pathologies can be assessed using multimodal CT including CT angiography, CT perfusion, and multimodal MRI.28,34,35 Immediate diagnostic imaging is suggested with the following clinical circumstances: when there is indication for fibrinolysis or anticoagulation therapy, history of bleeding tendencies, declining level of consciousness, symptoms that fluctuate, headache reported with stroke onset, stiff neck, papilledema, and fever.27–29 A prompt CT scan is necessary to rule out hemorrhage. When the patient is a candidate for fibrinolytic therapy such as tissue-type plasminogen activator (t-PA), noncontrast CT imaging should be completed within 25 minutes of arrival to the ED; interpretation should be completed no longer than 20 minutes after the CT scan.28
Fibrinolytic agents are used to dissolve the blood clot that is interrupting blood flow to the brain. Guidelines for the administration of fibrinolytic agents are established by The American Heart Association/American Stroke Association (AHA/ASA). These guidelines call for the initiation of fibrinolytic therapy up to 4.5 hours for patients who meet the inclusion criteria and present within 3 hours of stroke onset.37 Increased functional outcome and reperfusion are the benefits of receiving fibrinolytic therapy. One of the major risks for patients receiving fibrinolytic therapy is bleeding. The patient should be monitored for bleeding from I.V. sites, catheters, stool, urine, and nasogastric secretions. Eligibility criteria for t-PA include the following:27,29,36,37,38
- Age 18 years and older
- Diagnosis of ischemic stroke
- Onset of stroke less than 3 hours
- BP less than 185/110 mm Hg
- Not on an oral anticoagulant (warfarin)
- PT 15 seconds or less or INR 1.7 or less
- No seizure with stroke onset
- Not a minor or rapidly resolving stroke
- No prior surgical intervention within the past 14 days
- No gastrointestinal or urinary bleeding within the past 21 days.
- Without heparin in the past 48 hours
- No history of AVM, neoplasm, aneurysm, or intracranial hemorrhage.
- No stroke, serious head injury, or intracranial surgery within the last 3 months.
- No myocardial infarction within the last 3 months.
The recommended dosage for t-PA approved by the FDA is 0.9 mg/kg of body weight and is not to exceed a maximum dose of 90 mg. Ten percent of the dose can be administered as a bolus over 1 minute, and the remaining infused over 60 minutes.39,40
Other pharmacologic treatment
- Aspirin administration within 24 hours for patients with ischemic stroke without intracerebral hemorrhage.
- Anticoagulation therapy, heparin, and warfarin for acute venous stroke.
- Antiplatelets or anticoagulants for stroke secondary to acute arterial dissection.
- Prothrombin and vitamin K for hemorrhagic stroke to return clotting levels to normal.24,25
A stroke can leave patients with a high incidence of physical and psychosocial impairments. High-risk patients require education to identify and respond to early symptoms. Institutions must have clinical protocols and pathways to efficiently implement stroke therapies.
1. Miniño AM, Murphy SL, Xu J, Kochanek KD.Death Final Data for 2008 National Vital Statistics Reports; vol 59 no 10. Hyattsville, MD: National Center for Health Statistics; 2011.
2. Roger VL, Go AS, Lloyd-Jones DM, et al.Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012;125(1):e2–e20.
3. Heidenreich PA, Trogdon JG, Khavjou OA, Butler J, Dracup K, Ezekowitz MD, et al.Forecasting the future of cardiovascular disease in the United States: a policy statement from the American Heart Association. Circulation. 2011;123(8):933–944.
5. CDC. Health, United States, 2008. Hyattsville, MD: National Center for Health Statistics; 2008.
8. Treadwell SD, Robinson TG.Cocaine use and stroke. Postgrad Med J. 2007;83(980):389–394.
9. Hankey GJ.Nutrition and the risk of stroke. Lancet Neurol. 2012;11(1):66–81.
10. Shah RS, Cole JW.Smoking and stroke: the more you smoke the more you stroke. Expert Rev Cardiovasc Ther. 2010;8(7):917–932.
11. Arboix A, Alio J.Cardioembolic stroke: clinical features, specific cardiac disorders and prognosis. Curr Cardiol Rev. 2010;6(3):150–161.
12. Giles MF, Flossman E, Rothwell PM.Patient behavior immediately after transient ischemic attack according to clinical characteristics, perception of the event and predicted risk of stroke. Stroke. 2006;37(5):1254–1260.
13. Rothwell PM, Buchan A, Johnston SC.Recent advances in management of transient ischemic attacks and minor ischaemic strokes. Lancet Neurol. 2006;5(4):323–331.
14. National Institute of Neurological Disorders and Stroke, Stroke hope through research. 2011. http://www.ninds.nih.gov/disorders/stroke/detail_stroke.htm#appendix
15. Brouns R, De Deyn PP.The complexity of neurobiological process in acute ischemic stroke
. Clin Neurol Neurosurg. 2009;111(6):483–495.
16. Chavez JC, Hurko O, Barone FC, Feuerstein GZ.Pharmacologic interventions for stroke: Looking beyond the thrombolysis time window into the penumbra with Biomarkers, not a stopwatch. Stroke. 2009;40(10):e558–e563.
17. Yew K, Cheng E.Acute stroke diagnosis. Am Fam Physician. 2009;80(1):33–40.
18. Tocco S.Identify the vessel recognize the stroke. American Nurse Today. 2011;6(9):8–11.
20. Slater D.Middle cerebral artery stroke: Overview of middle cerebral artery stroke. Medscape. http://emedicine.medscape.com/article/323120-overview
21. Brugerolle B.International encyclopedia of rehabilitation. http://cirrie.buffalo.edu/encyclopedia/en/article/348/
23. Helseth E.Posterior cerebral artery stroke overview of PCA stroke. Medscape. http://emedicine.medscape.com/article/1160677-overview#aw2aab6b6
24. Kaye V.Vertibrobasilar stroke overview of vertibrobasilar stroke. Medscape. http://emedicine.medscape.com/article/323409-overview#aw2aab6b2
26. Oliveira-Filo J, Koroshetz W.Initial assessment and management of acute stroke. 2011. http://www.uptodate.com
27. Wechsler LR.Intravenous thrombolytic therapy for acute ischemic stroke
. N Engl J Med. 2011;364(22):2138–2146.
28. Adams HP Jr., del Zoppo G, Alberts MJ, et al.Guidelines for the early management of adults with ischemic stroke
: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. 2007;38(5):1655–1711.
29. National Institute for Health and Clinical Excellence (NIHCE). Stroke: Diagnosis and Initial Management of Acute Stroke and Transient Ischemic Attack (TIA). London, UK: Royal College of Physicians; 2008
30. Hinkle JL, Guanci MM.Acute ischemic stroke
review. J Neurosci Nurs. 2007;39(5):285–293, 310.
31. Summers D, Leonard A, Wentworth D, et al.Comprehensive overview of nursing and interdisciplinary care of the acute ischemic stroke
patient. Stroke. 2009;40(8):2911–2944
32. Kistler JP, Furie KL &, Hakan A.Initial evaluation and management of transient ischemic attack and minor stroke. In: BD Rose, ed. Waltham, MA: UpToDate. http://www.uptodate.com/online/content/topic.do?topicKey=cva_dise/6023&selectedTitle=1%7E150&source=search_result
33. Merino JG, Warach S.Imaging of acute Stroke. Nat Rev Neurol. 2010;6(10):560–571.
34. Sen S.Magnectic resonance imagining in acute stroke. Medscape. http://emedicine.medscape.com/article/1155506-overview#a1
35. Warren DJ, Musson R, Connoly DJ, Griffiths PD, Hoggard N.Imaging in acute ischemic stroke
: essential for treatment of modern stroke. Postgrad Med J. 2010;86(1017):409–418.
36. Hacke W, Kaste M, Bluhmki E, Brozman M, Dávalos A, Guidetti D, et al.Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke
. N Engl J Med. 2008;359(13):1317–1329.
37. Del Zoppo GJ, Saver JL, Jauch EC, Adams HP Jr.Expansion of the time window for treatment of acute ischemic stroke
with intravenous tissue plasminogen activator: a science advisory from the American Heart Association/American Stroke Association. Stroke. 2009;40(8):2945–2948.
38. Wahlgren N, Ahmed N, Dávalos A, et al.Thrombolysis with alteplase 3–4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. 2008;372(9646):1303–1309.
39. Nakagawara J, Minematsu K, Okada Y, et al.Thrombolysis with 0.6 mg/kg in- travenous alteplase for acute ischemic stroke
in routine clinical practice: the Ja- pan post-Marketing Alteplase Registration Study (J-MARS). Stroke. 2010;41(9):1984–1989.
40. Yamaguchi T, Mori E, Minematsu K, et al.Alteplase at 0.6 mg/kg for acute ischemic stroke
within 3 hours of onset: Japan Alteplase Clinical Trial (J-ACT). Stroke. 2006;37(7):1810–1815.