Acute Stroke

Chapter 6 Acute Stroke





Stroke Facts







Deaths from stroke can be reduced or delayed by preventing and controlling risk factors. Nonmodifiable risk factors for stroke include older age, family history of stroke or cardiovascular disease, male gender, and ethnicity (higher rates are seen in African Americans compared with whites). Modifiable risk factors include alcohol consumption, asymptomatic carotid bruit/stenosis, cardiac disease, cigarette smoking, diabetes mellitus, dyslipidemia, hypercoagulopathy, hypertension, illicit drug use, increased fibrinogen, obesity, oral contraceptive use, prior history of stroke, and transient ischemic attacks. Other factors may affect the risk of stroke. Because stroke deaths tend to occur more often during extremely hot or cold weather, season and climate may increase the risk of stroke. People of lower income and educational levels may also be at increased risk for stroke.



Classification of Stroke by Anatomic Location


Eighty percent of blood flow to the brain is supplied by the carotid arteries. Twenty percent is supplied through the vertebrobasilar system (Figure 6-1). Strokes involving the carotid arteries are called anterior circulation strokes or carotid territory strokes. They usually involve the cerebral hemispheres. Strokes affecting the vertebrobasilar arteries are called posterior circulation strokes or vertebrobasilar territory strokes. They usually affect the brain stem or cerebellum. Approximately 75% to 80% of ischemic strokes occur in the carotid (or anterior) circulation and 20% to 25% occur in the vertebrobasilar (or posterior) circulation.3 Signs and symptoms of stroke are shown in Table 6-1.



Table 6-1 Signs and Symptoms of Stroke



























Affected Artery Structures Supplied by Affected Vessel Signs and Symptoms of Blockage
Anterior cerebral Supplies medial surfaces and upper portions of frontal and parietal lobes





Middle cerebral (most commonly blocked vessel in stroke) Supplies a portion of the frontal lobe, lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand, and arm and in the dominant hemisphere, the areas for speech





Posterior cerebral Supplies medial and inferior temporal lobes, medial occipital lobe, thalamus, posterior hypothalamus, visual receptive area


Internal carotid Supplies cerebral hemispheres and diencephalon






Vertebral or basilar Supplies brainstem and cerebellum















Ischemic and Hemorrhagic Stroke




Ischemic Stroke


Of the approximately 795,000 strokes that occur each year, about 87% are ischemic, 10% are intracerebral hemorrhage, and 3% are subarachnoid hemorrhage.2,4 About 8% to 12% of ischemic strokes result in death within 30 days.3


There are two types of ischemic strokes: thrombotic and embolic. It is estimated that about 45% of ischemic strokes are caused by a small (~25%) or large artery (~20%) thrombus, about 20% are embolic in origin (most often from atrial fibrillation),5 and about 30% have an unknown cause.6


A thrombotic stroke is the most common cause of stroke (Figure 6-2). In a thrombotic stroke, atherosclerosis of large vessels in the brain causes progressive narrowing and platelet clumping. Platelet clumping results in the development of blood clots within the brain artery itself (i.e., cerebral thrombosis). When the blood clots are of sufficient size to block blood flow through the artery, the area that was previously supplied by that artery becomes ischemic. Ischemia occurs because the tissue supplied by the blocked artery does not receive oxygen and the essential nutrients needed for normal brain function. The patient’s signs and symptoms depend on the location of the artery affected and the areas of brain ischemia.




In an embolic stroke, material from an area outside the brain (e.g., heart, aorta, other major artery) becomes dislodged and travels through the bloodstream to the brain (i.e., cerebral embolism). Embolic material may consist of fragments of valves, tumors, or plaques; air; fat; amniotic fluid; a foreign body; or a blood clot. An embolus tends to become lodged where arteries branch because blood flow is most turbulent in these areas. Fragments of the embolus may become lodged in smaller vessels. As with thrombotic strokes, the patient’s signs and symptoms depend on the location of the artery affected and the areas of brain ischemia.




Evolution of an Ischemic Stroke


Complete blockage of an artery may lead to death of an area of cells in the brain because blood flow is obstructed (ischemic infarction). The evolution of the thrombosis may take place in a few minutes, hours, or even days. Large blood vessels, such as the carotid, middle cerebral, and basilar arteries, can take longer to become blocked than smaller vessels.


In an ischemic stroke, there are two main areas of injury (Figure 6-3). The first area is the zone of ischemia. Because of the blockage in the artery, there is little blood flow through this area. As a result, brain tissue previously supplied by the blocked vessel is deprived of oxygen, glucose, and other essential nutrients. Unless blood flow is quickly restored, nerve cells and other supporting nervous system cells will be irreversibly damaged or die (i.e., infarct) within a few minutes of the blockage.



Brain damage may occur because of the infarction as well as an excessive buildup of fluid in the brain (cerebral edema). As brain tissue dies, fluid begins to build up, resulting in swelling. Because the skull is a rigid container, as swelling increases, nearby brain tissue (nerve cells, nerve tracts, and cerebral arteries) is compressed, and intracranial pressure (ICP) increases. A sustained increase in pressure causes continued ischemia, irreparable damage to brain cells, and potentially death. Cerebral edema usually peaks 2 to 5 days after the onset of the stroke. The fluid buildup then stabilizes and may begin to decrease.


The second area of injury is called the ischemic penumbra or the transitional zone. The penumbra is a rim of brain tissue that surrounds the zone of ischemia. It is supplied with blood by collateral arteries that connect with branches of the blocked vessel. The size of the penumbra depends on the number and patency of the collateral arteries. Blood flow to brain tissue in this area is decreased to between 20% and 50% of normal, but not absent. Brain tissue in the penumbra is “stunned” but not yet irreversibly damaged. Because the collateral blood supply is not enough to maintain the brain’s demand for oxygen and glucose indefinitely, brain cells in the penumbra may live or die depending on how quickly blood flow is restored during the early hours of a stroke. Many acute stroke therapies are targeted toward restoring flow or function to the ischemic penumbra.11


A patient may experience warning signs of impending stroke. A transient ischemic attack (TIA) is one of the most important warning signs. A transient ischemic attack has been traditionally defined as a neurologic deficit caused by focal brain ischemia that completely resolves within 24 hours. Most TIAs last only about 5 to 20 minutes.3 This definition has been changed to “a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour, and without evidence of acute infarction.”12 This definition is tissue based rather than time based because some patients with traditionally defined transient ischemic attacks have, in fact, had a stroke.12 Some studies have shown positive magnetic resonance imaging (MRI) findings of stroke in up to two thirds of patients with a clinical transient ischemic attack diagnosis. The longer the duration of symptoms, the more likely that the MRI result will be positive.12 A TIA should be treated with the same urgency as a completed stroke.




Reperfusion Therapy


The time from the onset of stroke symptoms to treatment is a key factor to the success of any therapy. The earlier the treatment for stroke is given, the more favorable the results are likely to be. Blood flow needs to be restored to the affected area as quickly as possible. In acute stroke management, the phrase time is brain reflects the need for rapid assessment and intervention because delays in diagnosis and treatment may leave the patient neurologically impaired and disabled.13


Intravenous administration of a recombinant form of tissue plasminogen activator (rtPA) has proved to be an effective cerebral reperfusion therapy. Since 1996, the window of opportunity for the use of intravenous rtPA for the treatment of ischemic stroke patients has been within 3 hours of symptom onset. This has required that patients be at a hospital within 60 minutes of symptom onset to be evaluated and receive treatment. Unfortunately, delay in seeking treatment is a common reason for ineligibility for rtPA. Patients not directly seeking medical attention and waiting to see if their symptoms would improve; delays in transfer to a hospital capable of treating the patient; and indeterminate time of symptom onset are among the reasons for treatment delays, precluding the use of rtPA.14,15 The designation of a longer time window for treatment is one of the potential approaches that have been proposed to increase patient treatment opportunities.




Hemorrhagic Stroke


A hemorrhagic stroke is caused by either rupture of an artery with bleeding into the spaces surrounding the brain (i.e., subarachnoid hemorrhage) or bleeding into the brain tissue (i.e., intracerebral hemorrhage) (Figure 6-4). Hemorrhagic strokes can occur in patients of any age. When they occur in young patients, they generally are caused by the rupture of an aneurysm or an arteriovenous malformation. Rarely do these patients have a history of hypertension.




Subarachnoid Hemorrhage


Subarachnoid hemorrhage (SAH) accounts for about 3% of all strokes.4 A ruptured cerebral aneurysm is the most common cause of SAH. Patients often report a sudden onset “thunderclap” headache or describe the feeling as “the worst headache of my life.” Assessment findings and symptoms may quickly progress to forceful vomiting (often without nausea), neurologic deficits, and visual disturbances (e.g., blurry or double vision), unconsciousness, and seizures. The patient also may show signs and symptoms of rising intracranial pressure, such as unilateral pupil dilation, nausea, vomiting, and vital sign changes.


Initial mortality is high and rebleeding is common. Mortality from rebleeding is also high. Rebleeding most commonly occurs during the first day, usually within 12 hours of the initial hemorrhage.



Intracerebral hemorrhage


Intracerebral hemorrhage (ICH) accounts for about 10% of all strokes.4 Most intracerebral hemorrhages are associated with chronic hypertension, but other common causes and risk factors include bleeding disorders, African-American ethnicity, advanced age, vascular malformations, excessive use/abuse of alcohol, and liver dysfunction.16 This type of stroke may require neurosurgery.



You Should Know


Stroke care consists of two phases.16 Phase 1 (emergency or hyperacute phase) encompasses the first 3 to 24 hours after stroke onset and includes prehospital and emergency department care. During this phase, attention is focused on identifying stroke symptoms and location of the infarction, evaluating the patient’s risk for acute and long-term complications, and identifying treatment options. Phase 2 (acute care) encompasses the period 24 to 72 hours after stroke onset. This phase focuses on confirming the cause of stroke and preventing medical complications, preparing the patient and family for discharge, and establishing long-term secondary prevention measures.


Jul 10, 2016 | Posted by in RESPIRATORY | Comments Off on Acute Stroke

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