Ischemic Stroke

Ischemic Stroke

1. Treatment

   • Surgical
     • MERCI retriever (Lewis et al., 2011).
     • Carotid endarterectomy (Lewis et al., 2011).
     • Repair of aneurysm (Lewis et al., 2011).
     • Removal of tutor (Lewis et al., 2011).
     • Drainage of hematoma (Lewis et al., 2011).
     • Burr hole (Lewis et al., 2011).
     • Angioplasty (Lewis et al., 2011).
   • Pharamcological
     • Thromolytic; lyse (break down) existing clots i.e. Streptokinase, t-PA, rTpa
       • tPA
         • Must be administered within 3 to 4.5 hours of the onset of clinical signs of ischemic stroke (Lewis et al., 2011).
           • Administered IV to re-establish blood flow through a blocked artery to prevent cell death (Lewis et al., 2011).
         • The door-to-needle time for tPA remains less than 60 mins or 1 hour after onset of clinical signs. Thrombolytics given in this time frame reduce disability, but at the expense of an increase in deaths within 7 to 10 days and an increase in intracranial hemorrhage (Lewis et al., 2011).
     • Anticoagulants; Inhibit platelet aggregation, prevent platelet plugs e.g. ASA, Plavix
       • No anticoagulant or antiplatelet drugs are given for 24 hours after tPA treatment (Lewis et al., 2011).
       • Not recommended in the emergency phase because of the risk for intracranial hemorrhage (Lewis et al., 2011).
       • Aspirin at a dose of 325 mg may be initiated within 24 to 48 hours after the onset of an ischemic stroke
         • Complications of aspirin: GI bleeding. Therefore used cautiously in those who have a history of peptic ulcer disease (Lewis et al., 2011).
     • Antiplatelets
       • Used only after patient’s condition has been stabilized and to prevent further clot formation (Lewis et al., 2011).
     • Vasodilators (Lewis et al., 2011).
     • Anti-hyperlipidemics (Lewis et al., 2011).
     • Anti-hypertensives e.g. metoprolol
       • Hypertension may be a protective response to maintain cerebral perfusion
         • Use of drugs to lower BP is recommended only if BP is markedly increased (MAP>130 mm Hg or systolic BP>220 mm Hg) (Lewis et al., 2011).

2. Signs and Symptoms

   • Cognitive (Ignatavicius & Workman, 2013).
     • Denial of illness
     • Spatial and proprioveptive dysfunction
     • Impairment of memory, judgment, problem solving, and decision making
     • Decreased concentration
   • Motor (Ignatavicius & Workman, 2013).
     • Hemiplegia (paralysis) or hemiparesis (weakness) contralateral to which part of the brain is affected
     • Quadriparesis if the brainstem is involved
     • Ataxia (gait) if the cerebellum is affected
     • Hypotonia or flaccid paralysis
     • Hypertonia or spastic paralysis
     • Agnosia: unable to use objects correctly
     • Apraxia: unable to carryout purposeful motor activity or speech
     • Bladder and bowel incontinence from the loss of neurological control in the cerebral cortex
   • Sensory (Ignatavicius & Workman, 2013).
     • Decreased sensation of touch and pain contralateral to where the stroke is in the brain
     • Unilateral body neglect syndrome
     • Amaurosis fugax: brief episode of blindness in one eye
     • Hemiaopsia: blindness in half the visual field
     • Homonymous hemianopsia blindness in the same side of both eyes
     • Nystagmus: or other involuntary eye movements caused from brainstem and cerebellar damage
   • Cranial Nerve Dysfunction (Ignatavicius & Workman, 2013).
     • CN V: absent gag reflex and ability to chew
     • CN IX and X: decreased ability to swallow
     • CN XII: impaired tongue movement
     • CN VII: facial paralysis
   • Cardiovascular (Ignatavicius & Workman, 2013).
     • Embolic strokes are associated with heart murmurs, dysrhythmias (atrial fibrillation is the most common, and HTN.
   • Left vs. Right Hemisphere (Ignatavicius & Workman, 2013).

3. What is an ischemic stroke?

   • Ischemic stroke is caused by occlusion of cerebral artery by either a thrombus or embolus (Lewis et al., 2010).
     • Brain stores no oxygen or glucose and thus needs constant blood flow for normal function and waste removal (Lewis et al., 2010).
   • Stroke ranks third for mortality rates in developed countries (Kearney, 2014).

4. Pathophysiology

   • Thrombic Stokes
     • Consists of more than half of all strokes (Ignatavicius & Workman, 2013).
     • Caused by the development of atherosclerosis (Ignatavicius & Workman, 2013).
       • A rupture of one of these plaques exposes cells to clot promoting elements (Ignatavicius & Workman, 2013).
         • End result is a formation of a blood clot in an artery supplying blood to the brain. This blood clot is large enough to interrupt blood flow to cerebral tissue (Ignatavicius & Workman, 2013).
     • Thrombic strokes are characterized by a slow onset, taking minutes to hours (Ignatavicius & Workman, 2013).
   • Embolic Strokes
     • Caused by thrombus or thrombi breaking off an artery anywhere in the body and traveling to cerebral arteries (Ignatavicius & Workman, 2013).
       • Thrombus formation can be caused from heart disease, MI, heart valve prosthetics, non valvular atrial fibrillation, and plaque (Ignatavicius & Workman, 2013).
     • Embolic strokes are characterized by a sudden development, rapid neurological deficits (Ignatavicius & Workman, 2013).
     • Can lead to hemorrghaic stroke because arterial vessel wall is vulnerable to ischemic damage (Ignatavicius & Workman, 2013).

5. Diagnostic Tests

   • Laboratory Values
     • Elevated hematocrit and hemoglobin with severe or major stroke because body is compensating for decreased oxygen to the brain (Ignatavicius & Workman, 2013).
     • PT, PTT, and INR: used to establish baseline information for anticoagulation therapy (Ignatavicius & Workman, 2013).
     • Elevated WBC: can indicate presence of infection (Ignatavicius & Workman, 2013).
     • Lumbar puncture: used to rule out meningitis and subarachnoid hemmorhage (Ignatavicius & Workman, 2013).
   • Imaging Studies
     • MRI: to determine the extent of brain injury and has greater specificity in determining the location of vascular lesions and blockages than CT (Jauch, 2016).
     • CT scan: indicates the size and location of the lesion and helps to differentiate between ischemic and hemorrhagic stroke (Jauch, 2016).
     • Ultrasonography and echocardiography: help determine additional cardiovascular risks (Jauch, 2016).

6. Risk Factors

   • Modifiable (Choudhury et al., 2015; Ignatavicius & Workman, 2013).
     • Hypertension and atherosclerosis
     • Cardiovascular disease (i.e. atrial fibrillation)
     • Diabetes and glucose metabolism
     • High cholesterol levels
     • Smoking
     • Alcohol consumption
     • Illicit drug use (particularly cocaine)
     • Lifestyle factors (i.e. obesity, physical activity diet)
     • Sleep apnea
     • Blood clotting disorders (high risk for thrombotic stroke and require preventive anticoagulants)
     • TIA patients (should seek anticoagulation therapy)
   • Non modifiable (Choudhury et al., 2015; Ignatavicius & Workman, 2013).
     • Age; increased risk as age increases
     • Gender; men 30% higher incidence, post menopausal women
     • Race or ethnicity; American Indian, Alaskan Natives, Blacks, Hispanics have a higher chance
     • Heredity
     • Myocardial Infarction
     • Sickle Cell Disease

7. Collaborative Care

   • Nursing
     • Managing circulation, airway, breathing → Patients may have difficulty keeping an open and clear airway because of a decreased LOC or decreased or absent gag and swallowing reflexes (Lewis et al., 2011).
     • Oxygenation
       • Maintaining oxygenation is important - Both hypoxia and hypercarbia are to be prevented because they can contribute to secondary neuronal injury (Lewis et al., 2011).
       • Oxygen administration, artificial airway insertion, intubation, and mechanical ventilation may be required (Lewis et al., 2011).
     • Neurological Assessment
       • Glasgow Coma Scale to address LOC, orientation, motor, pupils, speech.language, vital signs, and blood glucose (RNAO, 2005).
     • Fluid and electrolytes
       • keep the patient adequately hydrated to promote perfusion and decrease further brain injury (Lewis et al., 2011).
       • Adequate fluid intake during acute care via oral, IV, or tube feedings should be 1500 to 2000 mL/day (Lewis et al., 2011).
       • IV solutions and water ware avoided because they are hypotonic and may further increase cerebral edema and ICP(Lewis et al., 2011).
       • Hyperglycemia may be associated with further brain damage and should be treated (Lewis et al., 2011).
     • Management of Increased ICP
       • Improve venous drainage (i.e. elevate HOB)
       • Maintain head and neck in alignment (Lewis et al., 2011).
       • Quiet environments will reduce headaches and reduce aggravation of increased ICP (Ignatavicius & Workman, 2013).
       • Avoid extreme hip and neck flexions that increase intrathoracic pressure making ICP more difficult to control. Extreme neck flextion interferes with venous drainage as well (Lewis et al., 2011).
       • Avoid clustering nursing procedures all at once because the effect of ICP elevation is more dramatic (Ignatavicius & Workman, 2013).
       • CSF drainage (Ignatavicius & Workman, 2013).
       • Diuretic drugs (e.g. mannitol, furosemide) (Lewis et al., 2011).
       • Removal of bone flap to allow for cerebral edema without increases in ICP (Lewis et al., 2011).
     • Management of Constipation
       • Constipation can be caused from decreased mobility (Kasaeaneni & Hayes, 2014).
       • High fiber food such as fruits or vegetables can be added to the diet to help increase the volume present and cause bowel movement by distension (Kasaeaneni & Hayes, 2014).
       • Fiber supplements such as bran, psyllium, or methylcellulose can be added to help increase the fiber consumed by the patient (Kasaeaneni & Hayes, 2014).
       • Encourage fluid intakes (Kasaeaneni & Hayes, 2014).
     • Avoid Hyperthermia
       • Contributes to increased cerebral metabolism. A temperature elevation of even one degree increases brain metabolism by 10% and contribute to further brain damage (Lewis et al., 2011).
       • Treatment: Aspirin Acetaminophen Cool blankets (Lewis et al., 2011).
     • Education
       • Teach patients to recognize the symptoms of a stroke by using the acronym FAST
       • Return demonstrations assist in evaluating family' ability to perform patient care tasks; provide verbal and oral instruction Ignatavicius & Workman, 2013).
       • Teach family about depression that can occur within 3 months of a stroke. Post stroke depression is associated with increased morbidity (Ignatavicius & Workman, 2013).
       • Health teaching for the patient includes drug therapy, ambulation skills, nutritional management, and self management skills (Ignatavicius & Workman, 2013).
       • Health Care Resources (Ignatavicius & Workman, 2013)
         • Available online resources to share with patients and family include American Heart Association, National Stroke Association, Agency of Health care Research and Quality
   • SLP (Speech Language Pathologist)
     • Appointments for outpatients speech may be arranged to help the patient relearn to talk (Ignatavicius & Workman, 2013).
     • Collaborate with the SLP to conduct a bedside swallowing screening and evaluation. Patient may remain NPO until SLP determines the patient can tolerate fluids without aspirating (Ignatavicius & Workman, 2013).
   • Home
     • Collaborate with case manager to plan patient's discharge; coordinate with rehabilitation therapist to identify need of assistive devices (Ignatavicius & Workman, 2013).
       • PT (Physiotherapist)
         • To restore movement, balance, and coordination
           • Climb stairs, transfer in and out of bed and chair, transfer to and from car, mobility aids (Ignatavicius & Workman, 2013).
       • OT (Occupational Therapist)
         • To relearn basic skills such as bathing and dressing
   • Community Care
     • Patients with stroke may be discharged to a rehabilitation centre or skilled nursing fac.ility depending on the extent of their disability and the availability of caregiver/family support (Ignatavicius & Workman, 2013).

8. Complications

   • Increase ICP
     • Occurs in response to cerebral edema (American Heart Association, 2015).
   • Pneumonia
     • Due to decreased mobility after a stroke (American Heart Association, 2015).
     • Aspiration pneumonia
       • Can be caused by impaired tongue movement, decreased swallowing, or absent gag reflex (American Heart Association, 2015).
   • Urinary Tract Infection
     • Caused by foley catheter being placed due to bladder incontinence (American Heart Association, 2015).
   • Seizure
     • Abnormal electrical activity in the brain causing convulsions from cerebral damage (American Heart Association, 2015).
   • Clinical depression
     • Causes unwanted emotional and physical reactions to changes and losses (American Heart Association, 2015).
   • Pressure ulcers
     • Results from decreased ability to move and pressure on areas of the body because of immobility (American Heart Association, 2015).
   • Limb contractures
     • Shortened muscles in an arm or leg from reduced ability to move the affected limb or lack of exercise (American Heart Association, 2015).
   • Deep Vein Thrombosis
     • Blood clots form in veins of the legs because of immobility from stroke. (American Heart Association, 2015).

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