View Entire Collection
By Clinical Topic
By State Requirement
Diabetes – Summer 2012
Faith Community Nursing
Fluids & Electrolytes
Future of Nursing Initiative
Heart Failure - Fall 2011
Influenza - Winter 2011
Nursing Ethics - Fall 2011
Trauma - Fall 2010
Traumatic Brain Injury - Fall 2010
Stroke strikes suddenly. Find out how to act fast to prevent or lessen neurologic deficits.
Every year, about 700,000 Americans experience a new or recurrent stroke. And every 3 minutes, someone dies from the event.1 Because the brain's metabolic demands are high compared with other organs, permanent damage can occur within minutes if blood supply is interrupted.
Strokes are classified according to type:
* Ischemic strokes are caused by an obstruction of cerebral blood flow, often from intracranial arteriosclerosis, carotid plaque with arteriogenic emboli, flow-reducing carotid stenosis, or aortic arch plaque. An embolus caused by atrial fibrillation or valvular heart disease, for example, also can travel from the heart to the brain and cut off blood supply.
* Hemorrhagic strokes result from a vessel rupturing and bleeding into the brain or spaces around the brain. Causes include aneurysm rupture, uncontrolled hypertension, subarachnoid hemorrhage, infection, clotting disorders, trauma or radiation to the head or neck, and cerebral angioplasty.
Because stroke manifestations depend on the affected vessel or area, you'll need to understand the brain's circulation.
The carotid arteries supply 80% of the cerebral blood flow, with the vertebral arteries supplying the remaining 20%. The internal carotid arteries supply the anterior and middle parts of the cerebral hemispheres.
The vertebrobasilar arteries supply the posterior parts of the cerebral hemispheres, the brain stem, and the cerebellum.
The circle of Willis sits at the base of the brain, and is a ring of joined vessels that receives blood from the internal carotid and vertebrobasilar arteries. The arteries in this circle are:
* the anterior cerebral artery, which supplies the medial surface of the frontal and parietal lobes.
* the middle cerebral arteries, which supply the lateral surfaces of the cerebral hemispheres and have smaller branches that take blood flow deeper into the brain's structure.
* the posterior cerebral arteries, which supply the medial and inferior surfaces of the occipital and temporal lobes.
The brain's vascular system automatically changes the diameter of its vessels to maintain a constant cerebral blood flow during blood pressure (BP) fluctuations-a process known as autoregulation. The brain can effectively autoregulate when systolic BP is 60 to 100 mm Hg. But when autoregulation fails, cerebral blood flow diminishes, resulting in ischemia.2
For details on the parts of the brain and the functions they handle, see Getting cerebral.
Stroke signs and symptoms vary according to the location of the blood supply deficit. Signs and symptoms are sudden and can range from local manifestations on one side of the body to deep coma.
A left cerebral hemisphere stroke results in weakness, numbness, or neglect on the body's right side. If the speech-controlling Broca's area is affected, the patient will have aphasia (expressive, receptive, or mixed). His face will be asymmetrical on the right, and he may lose vision in the right visual field of both eyes.
If the patient's brain stem and cerebellum are affected, he may experience hemi- or quadriparesis, hemisensory loss and ataxia, abnormal eye movements, oropharyngeal weakness, nausea, vomiting, hiccups, vertigo, tinnitus, abnormal respirations, and decreased level of consciousness. An affected thalamic area results in sensory alterations (touch, pain, vibration, and temperature).
When you take the patient's medical history, he may describe transient ischemic attacks (TIAs)-brief losses of function that resolve within 24 hours. Patients who have a TIA must be evaluated promptly for stroke risk. According to the National Institute of Neurological Disorders and Stroke, about one-third of patients who have a TIA will have a stroke.3
Quick diagnosis and treatment is essential to preserving brain tissue and function. When your patient arrives at the emergency department, assess his level of consciousness and his ABCs. Next, ask him about his symptoms and when they started. Complete bedside neurologic assessments and the National Institutes of Health Stroke Scale to determine stroke severity. Obtain samples for lab tests, including a complete blood cell count, platelet count, coagulation studies, metabolic panel, and urinalysis. Carefully review blood glucose results; disturbances can mimic stroke. Also obtain an electrocardiogram to rule out cardiac dysrhythmias.
The single most effective tool to diagnose a stroke (and determine whether it's ischemic or hemorrhagic) is a nonenhanced computed tomography (CT) scan of the brain. Magnetic resonance imaging also may be ordered to help determine the exact location and size of injury; this test is especially helpful for assessing smaller strokes located deep in brain tissue.
An electroencephalogram can reveal the brain's electrical activity and helps screen for seizure activity resulting from brain injury. Carotid Doppler studies can help evaluate the patency of the carotid arteries.
Although nothing will stop a stroke from occurring, tissue plasminogen activator (t-PA) can minimize the size of the infarcted area by dissolving a clot and opening a blocked blood vessel. Patients 18 and older are eligible for t-PA therapy if they have a clinical diagnosis of ischemic stroke with a measurable neurologic deficit, and symptoms began less than 3 hours before treatment begins. Also, a pretreatment noncontrast head CT scan must show no evidence of intracranial bleeding, and the patient must meet all exclusion criteria contraindications.
Although t-PA therapy can improve outcomes, overall success rates remain low.4 This therapy isn't recommended for patients with isolated mild neurologic deficits, such as ataxia alone, or trace weakness.5
If t-PA is used, the recommended dose is 0.9 mg/kg, or a maximum of 90 mg, given over 60 minutes, with 10% of the total dose given as an initial I.V. bolus over 1 minute. Monitor the patient's vital signs and neurologic status, and monitor for bleeding complications for at least 24 hours after administering t-PA. Withhold anticoagulants and antiplatelets during this time also. A CT scan is usually done within 24 hours, and an emergent head CT scan is done if the patient's clinical status deteriorates during or after t-PA therapy.
If the patient isn't a candidate for t-PA, treatment focuses on signs and symptoms and the potential cause of the stroke. For example, a patient with a cardiac history may have atrial fibrillation, and would need anticoagulation once a hemorrhagic stroke is ruled out by CT scan.
If the patient is hypertensive and the stroke is caused by hemorrhage, surgery may be needed to evacuate the bleed (after his BP is controlled). The patient may receive an anticonvulsant medication as a prophylactic measure. The patient's BP is lowered slowly with medications to ensure adequate cerebral perfusion. If the patient has hyperlipidemia, anticholesterol medications can be started as soon as liver function is determined to be normal. To treat cerebral vasospasm, a calcium channel blocker is given to relax vascular smooth muscle and improve cerebral blood flow and neurologic function.
Monitor the patient for complications such as aspiration pneumonia, venous thromboembolism (VTE), pressure ulcers, malnutrition, and contractures. Keep the patient's airway patent and encourage deep breathing and coughing exercises, incentive spirometry, early mobility, and frequent position changes to help prevent atelectasis. If the patient develops signs of pneumonia (fever, chills, elevated white blood cell count, changes in breath sounds), notify the health care provider and expect orders for blood cultures, sputum culture, chest X-ray, and antibiotic therapy.
Evaluate swallowing early in the patient's admission to avoid aspiration. If he has trouble swallowing, keep him N.P.O. until you obtain a swallowing evaluation, which should be done within 24 hours. Obtain a nutritional consult to ensure that he meets his caloric needs.
Evaluate the patient's risk for VTE and institute prophylactic measures, including the use of low-dose unfractionated heparin or low-molecular-weight heparin, as prescribed. If anticoagulants are contraindicated, use mechanical prophylaxis with graduated compression stockings or intermittent pneumatic compression. Encourage him to move his extremities to prevent blood stasis and pressure ulcers.
Lifestyle changes may help a patient decrease stroke risk factors. Encourage him to eat a balanced diet; exercise regularly; control his BP, blood glucose, and lipid levels; and stop smoking, if appropriate.
By understanding stroke, you can help your patient recover and prevent future problems.
To understand the clinical presentation of stroke, you should have a basic understanding of neuroanatomy and function. The brain is divided into three main components:
* the cerebrum is the largest and most advanced part of the brain, responsible for higher intellect, speech, emotion, movement, and integration of sensory stimuli of all types. The cerebrum is divided into right and left hemispheres, each with a frontal, parietal, temporal, and occipital lobe. Because nerves cross in the brain stem, the left side of the brain controls the right side of the body and vice versa.
* the cerebellum is the second-largest part of the brain and is responsible for balance and coordination, and assists in controlling movement.
* the brain stem handles automatic functions, such as respiration, heart rate, blood pressure, wakefulness, arousal, and attention.
1. American Heart Association. Heart disease and stroke statistics: 2006 update. http://www.americanheart.org/downloadable/heart/1136308648540Statupdate2006.pdf. Accessed October 30, 2006. [Context Link]
2. Smeltzer SC, Bare BG. Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 9th edition. Philadelphia, Pa., Lippincott, Williams & Wilkins, 2000. [Context Link]
3. National Institute of Neurological Disorders and Stroke. http://www.ninds.nih.gov. Accessed October 30, 2006. [Context Link]
4. The University of Medicine and Dentistry of New Jersey and Millennium CME Institute. Acute Stroke Express Report-Providing the Latest in Evidence-Based Medicine March 30, 2004. CME Certified Monograph. Critical decisions in the emergency management of stroke. http://www.millennium-cme.com/reports/590-286-04-04-EC.pdf. Accessed October 30, 2006. [Context Link]
5. Fowler S. Acute stroke. Unpublished handouts. American Association of Neuroscience Nurses, May 20, 2004. [Context Link]
For life-long learning and continuing professional development, come to Lippincott's NursingCenter.
HIV infection and its implication for nurse leaders
Nursing Management, October 2014
Expires: 10/31/2016 CE:2 $21.95
Being Prepared: Bioterrorism and Mass Prophylaxis: Part I
Advanced Emergency Nursing Journal, July/September 2014
Expires: 9/30/2016 CE:2.5 $24.95
CE: A Mobility Program for an Inpatient Acute Care Medical Unit
AJN, American Journal of Nursing, October 2014
Expires: 10/31/2016 CE:2 $21.95
More CE Articles
Subscribe to Recommended CE
What internal motivators drive RNs to pursue a BSN?
Nursing2014 , October 2014
Free access will expire on November 24, 2014.
Breast Cancer Risk Assessment in Primary Care
MCN, The American Journal of Maternal/Child Nursing, September/October 2014
Free access will expire on November 10, 2014.
Nurses spurring innovation
Nursing Management, October 2014
Free access will expire on November 10, 2014.
More Recommended Articles
Subscribe to Recommended Articles
Back to Top