Ischemic Stroke.

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Presentation transcript:

Ischemic Stroke

An ischemic stroke, cerebrovascular accident (CVA), or “brain attack” is a sudden loss of function resulting from disruption of the blood supply to a part of the brain.. With the approval of thrombolytic therapy for the treatment of acute ischemic stroke in 1996 came a revolution in the care of patients after a stroke.

Ischemic strokes are subdivided into five different types based on the cause (1) large artery thrombotic strokes (20%) (2) small penetrating artery thrombotic strokes (25%), (3) cardiogenic embolic strokes (20%), (4) cryptogenic strokes (30%), (5) other (5%)

Large artery thrombotic strokes are caused by atherosclerotic plaques in the large blood vessels of the brain. Thrombus formation and occlusion at the site of the atherosclerosis result in ischemia and infarction (deprivation of blood supply). Small penetrating artery thrombotic strokes affect one or more vessels and are the most common type of ischemic stroke. Small artery thrombotic strokes are also called lacunar strokes because of the cavity that is created after the death of infarcted brain tissue.

Cardiogenic embolic strokes are associated with cardiac dysrhythmias, usually atrial fibrillation. Embolic strokes can also be associated with valvular heart disease and thrombi in the left ventricle. Emboli originate from the heart and circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented by the use of anticoagulation therapy in patients with atrial fibrillation.

The last two classifications of ischemic strokes are cryptogenic strokes, which have no known cause, and strokes from other causes, such as illicit drug use, coagulopathies, migraine, and spontaneous dissection of the carotid or vertebral arterie

Glossary agnosia failure to recognize familiar objects perceived by the senses aneurysm a weakening or bulge in an arterial wall aphasia inability to express oneself or to understand language

apraxia inability to perform previously learned purposeful motor acts on a voluntary basis ataxia impaired ability to coordinate movement, often seen as a staggering gait or postural imbalance

dysarthria defects of articulation due to neurologic causes expressive aphasia inability to express oneself; often associated with damage to the left frontal lobe area hemianopsia blindness of half of the field of vision in one or both eyes

hemiplegia/hemiparesis weakness/paralysis of one side of the body, or part or it, due to an injury to the motor areas of the brain infarction a zone of tissue deprived of blood supply Korsakoff's syndrome personality disorder characterized by psychosis, disorientation, delirium, insomnia, and hallucinations

penumbra region area of low cerebral blood flow receptive aphasia inability to understand what someone else is saying; often associated with damage to the temporal lobe area

Pathophysiology In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of a blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic events referred to as the ischemic cascade. The ischemic cascade begins when cerebral blood flow decreases to less than 25 mL per 100 g per minute. At this point, neurons are no longer able to maintain aerobic respiration. The mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in the pH level. This switch to the less efficient anaerobic respiration also renders the neuron incapable of producing sufficient quantities of adenosine triphosphate (ATP) to fuel the depolarization processes.

The membrane pumps that maintain electrolyte balances begin to fail, and the cells cease to function. Early in the cascade, an area of low cerebral blood flow, referred to as the penumbra region, exists around the area of infarction. The penumbra region is ischemic brain tissue that may be salvaged with timely intervention.

The ischemic cascade threatens cells in the penumbra because membrane depolarization of the cell wall leads to an increase in intracellular calcium and the release of glutamate. The influx of calcium and the release of glutamate, if continued, activate a number of damaging pathways that result in the destruction of the cell membrane, the release of more calcium and glutamate, vasoconstriction, and the generation of free radicals. These processes enlarge the area of infarction into the penumbra, extending the stroke. Each step in the ischemic cascade represents an opportunity for intervention to limit the extent of secondary brain damage caused by a stroke.

Clinical Manifestations An ischemic stroke can cause a wide variety of neurologic deficits, depending on the location of the lesion (which vessels are obstructed), the size of the area of inadequate perfusion, and the amount of collateral (secondary or accessory) blood flow. The patient may present with any of the following signs or symptoms:

Numbness or weakness of the face, arm, or leg, especially on one side of the body Confusion or change in mental status Trouble speaking or understanding speech Visual disturbances Difficulty walking, dizziness, or loss of balance or coordination Sudden severe headache

Motor, sensory, cranial nerve, cognitive, and other functions may be disrupted. reviews the neurologic deficits frequently seen in patients with strokes. compares the symptoms and behaviors seen in right hemispheric stroke with those seen in left hemispheric stroke.

Assessment and Diagnostic Findings Any patient with neurologic deficits needs a careful history and a complete physical and neurologic examination. Initial assessment focuses on airway patency, which may be compromised by loss of gag or cough reflexes and altered respiratory pattern; cardiovascular status (including blood pressure, cardiac rhythm and rate, carotid bruit); and gross neurologic deficits. Patients may present to the acute care facility with temporary neurologic symptoms. A transient ischemic attack (TIA) is a neurologic deficit lasting less than 24 hours, with most episodes resolving in less than 1 hour. A TIA is manifested by a sudden loss of motor, sensory, or visual function. The symptoms result from temporary ischemia (impairment of blood flow) to a specific region of the brain. A TIA may serve as a warning of impending stroke.

Lack of evaluation and treatment of a patient who has experienced previous TIAs may result in a stroke and irreversible deficits The initial diagnostic test for a stroke is a noncontrast computed tomography (CT) scan performed emergently to determine if the event is ischemic or hemorrhagic (the category of stroke determines treatment). Further diagnostic workup for ischemic stroke involves attempting to identify the source of the thrombi or emboli. A 12-lead electrocardiogram (ECG) and a carotid ultrasound are standard tests. Other studies may include cerebral angiography; transcranial Doppler flow studies; transthoracic or transesophageal echocardiography; magnetic resonance imaging (MRI) of the brain, neck, or both; xenon-enhanced CT scan; and single photon emission CT (SPECT) scan

Prevention Primary prevention of ischemic stroke remains the best approach. Stroke risk screenings are an ideal opportunity to lower stroke risk by identifying people or groups of people who are at high risk for stroke and by educating patients and the community about recognition and prevention of stroke). Recent research findings suggest that low-dose aspirin may lower the risk of stroke in women).

Advanced age, gender, and race are well-known nonmodifiable risk factors for stroke. High-risk groups include people older than 55 years of age; the incidence of stroke more than doubles in each successive decade. Men have a higher rate of stroke than women do. Another high-risk group is African Americans; . Many health promotion efforts encourage a healthy lifestyle with appropriate health maintenance; eating a low-fat, low-cholesterol diet; and increasing exercise.

Medical Management Patients who have experienced a TIA or stroke should have medical management for secondary prevention. Those with atrial fibrillation (or cardioembolic strokes) are treated with dose-adjusted warfarin sodium (Coumadin) unless contraindicated. The international normalized ratio (INR) target is 2.5. If warfarin is contraindicated, aspirin is the best option, although other medications may be used if both are contraindicated).

Modifiable Risk Factors for Ischemic Stroke Hypertension (controlling hypertension, the major risk factor, is the key to preventing stroke) Atrial fibrillation Hyperlipidemia Diabetes mellitus (associated with accelerated atherogenesis) Smoking Asymptomatic carotid stenosis Obesity Excessive alcohol consumption

Nursing Process The Patient Recovering From an Ischemic Stroke Assessment During the acute phase, a neurologic flow sheet is maintained to provide data about the following important measures of the patient's clinical status:

Change in level of consciousness or responsiveness as evidenced by movement, resistance to changes of position, and response to stimulation; orientation to time, place, and person Presence or absence of voluntary or involuntary movements of the extremities; muscle tone; body posture; and position of the head Stiffness or flaccidity of the neck Eye opening, comparative size of pupils and pupillary reactions to light, and ocular position Color of the face and extremities; temperature and moisture of the skin Quality and rates of pulse and respiration; arterial blood gas values as indicated, body temperature, and arterial pressure Ability to speak Volume of fluids ingested or administered; volume of urine excreted each 24 hours Presence of bleeding Maintenance of blood pressure within the desired parameters

Nursing Diagnoses Impaired physical mobility related to hemiparesis, loss of balance and coordination, spasticity, and brain injury Acute pain (painful shoulder) related to hemiplegia and disuse Self-care deficits (bathing, hygiene, toileting, dressing, grooming, and feeding) related to stroke sequelae Disturbed sensory perception related to altered sensory reception, transmission, and/or integration Impaired swallowing Total urinary incontinence related to flaccid bladder, detrusor instability, confusion, or difficulty in communicating Disturbed thought processes related to brain damage, confusion, or inability to follow instructions Impaired verbal communication related to brain damage Risk for impaired skin integrity related to hemiparesis, hemiplegia, or decreased mobility Interrupted family processes related to catastrophic illness and caregiving burdens Sexual dysfunction related to neurologic deficits or fear of failure

Collaborative Problems/Potential Complications Potential complications include: Decreased cerebral blood flow due to increased ICP Inadequate oxygen delivery to the brain Pneumonia

Planning and Goals Although rehabilitation begins on the day the patient has the stroke, the process is intensified during convalescence and requires a coordinated team effort. It is helpful for the team to know what the patient was like before the stroke: his or her illnesses, abilities, mental and emotional state, behavioral characteristics, and activities of daily living (ADLs). It is also helpful for clinicians to be knowledgeable about the relative importance of predictors of stroke outcome (age, NIHSS score, and level of consciousness at time of admission) in order to provide stroke survivors and their families with realistic goals The major goals for the patient (and family) may include improved mobility, avoidance of shoulder pain, achievement of self-care, relief of sensory and perceptual deprivation, prevention of aspiration, continence of bowel and bladder, improved thought processes, achieving a form of communication, maintaining skin integrity, restored family functioning, improved sexual function, and absence of complications

Nursing Interventions Improving Mobility and Preventing Joint Deformities Preventing Shoulder Adduction Positioning the Hand and Fingers Changing Positions Establishing an Exercise Program Preparing for Ambulation Preventing Shoulder Pain Enhancing Self-Care Nursing Research Profile Long-Term Pain After a Stroke Assisting With Nutrition Attaining Bowel and Bladder Control Improving Thought Processes Improving Communication Communicating With the Patient With Aphasia

Maintaining Skin Integrity Improving Family Coping Helping the Patient Cope With Sexual Dysfunction Promoting Home and Community-Based Care Teaching Patients Self-Care Continuing Care