Ischemic Stroke

Treatment
1. Surgical
  1. MERCI retriever (Lewis et al., 2011).
  2. Carotid endarterectomy (Lewis et al., 2011).
  3. Repair of aneurysm (Lewis et al., 2011).
  4. Removal of tutor (Lewis et al., 2011).
  5. Drainage of hematoma (Lewis et al., 2011).
  6. Burr hole (Lewis et al., 2011).
  7. Angioplasty (Lewis et al., 2011).
2. Pharamcological
  1. Thromolytic; lyse (break down) existing clots i.e. Streptokinase, t-PA, rTpa
    1. tPA
      1. 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).
      2. 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).
  2. Anticoagulants; Inhibit platelet aggregation, prevent platelet plugs e.g. ASA, Plavix
    1. No anticoagulant or antiplatelet drugs are given for 24 hours after tPA treatment (Lewis et al., 2011).
    2. Not recommended in the emergency phase because of the risk for intracranial hemorrhage (Lewis et al., 2011).
    3. Aspirin at a dose of 325 mg may be initiated within 24 to 48 hours after the onset of an ischemic stroke
      1. Complications of aspirin: GI bleeding. Therefore used cautiously in those who have a history of peptic ulcer disease (Lewis et al., 2011).
  3. Antiplatelets
    1. Used only after patient’s condition has been stabilized and to prevent further clot formation (Lewis et al., 2011).
  4. Vasodilators (Lewis et al., 2011).
  5. Anti-hyperlipidemics (Lewis et al., 2011).
  6. Anti-hypertensives e.g. metoprolol
    1. Hypertension may be a protective response to maintain cerebral perfusion
      1. 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).
Signs and Symptoms
1. Cognitive (Ignatavicius & Workman, 2013).
  1. Denial of illness
  2. Spatial and proprioveptive dysfunction
  3. Impairment of memory, judgment, problem solving, and decision making
  4. Decreased concentration
2. Motor (Ignatavicius & Workman, 2013).
  1. Hemiplegia (paralysis) or hemiparesis (weakness) contralateral to which part of the brain is affected
  2. Quadriparesis if the brainstem is involved
  3. Ataxia (gait) if the cerebellum is affected
  4. Hypotonia or flaccid paralysis
  5. Hypertonia or spastic paralysis
  6. Agnosia: unable to use objects correctly
  7. Apraxia: unable to carryout purposeful motor activity or speech
  8. Bladder and bowel incontinence from the loss of neurological control in the cerebral cortex
3. Sensory (Ignatavicius & Workman, 2013).
  1. Decreased sensation of touch and pain contralateral to where the stroke is in the brain
  2. Unilateral body neglect syndrome
  3. Amaurosis fugax: brief episode of blindness in one eye
  4. Hemiaopsia: blindness in half the visual field
  5. Homonymous hemianopsia blindness in the same side of both eyes
  6. Nystagmus: or other involuntary eye movements caused from brainstem and cerebellar damage
4. Cranial Nerve Dysfunction (Ignatavicius & Workman, 2013).
  1. CN V: absent gag reflex and ability to chew
  2. CN IX and X: decreased ability to swallow
  3. CN XII: impaired tongue movement
  4. CN VII: facial paralysis
5. Cardiovascular (Ignatavicius & Workman, 2013).
  1. Embolic strokes are associated with heart murmurs, dysrhythmias (atrial fibrillation is the most common, and HTN.
6. Left vs. Right Hemisphere (Ignatavicius & Workman, 2013).
What is an ischemic stroke?
1. Ischemic stroke is caused by occlusion of cerebral artery by either a thrombus or embolus (Lewis et al., 2010).
  1. Brain stores no oxygen or glucose and thus needs constant blood flow for normal function and waste removal (Lewis et al., 2010).
2. Stroke ranks third for mortality rates in developed countries (Kearney, 2014).
Pathophysiology
1. Thrombic Stokes
  1. Consists of more than half of all strokes (Ignatavicius & Workman, 2013).
  2. Caused by the development of atherosclerosis (Ignatavicius & Workman, 2013).
    1. A rupture of one of these plaques exposes cells to clot promoting elements (Ignatavicius & Workman, 2013).
      1. 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).
  3. Thrombic strokes are characterized by a slow onset, taking minutes to hours (Ignatavicius & Workman, 2013).
2. Embolic Strokes
  1. Caused by thrombus or thrombi breaking off an artery anywhere in the body and traveling to cerebral arteries (Ignatavicius & Workman, 2013).
    1. Thrombus formation can be caused from heart disease, MI, heart valve prosthetics, non valvular atrial fibrillation, and plaque (Ignatavicius & Workman, 2013).
  2. Embolic strokes are characterized by a sudden development, rapid neurological deficits (Ignatavicius & Workman, 2013).
  3. Can lead to hemorrghaic stroke because arterial vessel wall is vulnerable to ischemic damage (Ignatavicius & Workman, 2013).
Diagnostic Tests
1. Laboratory Values
  1. Elevated hematocrit and hemoglobin with severe or major stroke because body is compensating for decreased oxygen to the brain (Ignatavicius & Workman, 2013).
  2. PT, PTT, and INR: used to establish baseline information for anticoagulation therapy (Ignatavicius & Workman, 2013).
  3. Elevated WBC: can indicate presence of infection (Ignatavicius & Workman, 2013).
  4. Lumbar puncture: used to rule out meningitis and subarachnoid hemmorhage (Ignatavicius & Workman, 2013).
2. Imaging Studies
  1. 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).
  2. CT scan: indicates the size and location of the lesion and helps to differentiate between ischemic and hemorrhagic stroke (Jauch, 2016).
  3. Ultrasonography and echocardiography: help determine additional cardiovascular risks (Jauch, 2016).
Risk Factors
1. Modifiable (Choudhury et al., 2015; Ignatavicius & Workman, 2013).
  1. Hypertension and atherosclerosis
  2. Cardiovascular disease (i.e. atrial fibrillation)
  3. Diabetes and glucose metabolism
  4. High cholesterol levels
  5. Smoking
  6. Alcohol consumption
  7. Illicit drug use (particularly cocaine)
  8. Lifestyle factors (i.e. obesity, physical activity diet)
  9. Sleep apnea
  10. Blood clotting disorders (high risk for thrombotic stroke and require preventive anticoagulants)
  11. TIA patients (should seek anticoagulation therapy)
2. Non modifiable (Choudhury et al., 2015; Ignatavicius & Workman, 2013).
  1. Age; increased risk as age increases
  2. Gender; men 30% higher incidence, post menopausal women
  3. Race or ethnicity; American Indian, Alaskan Natives, Blacks, Hispanics have a higher chance
  4. Heredity
  5. Myocardial Infarction
  6. Sickle Cell Disease
Collaborative Care
1. Nursing
  1. 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).
  2. Oxygenation
    1. Maintaining oxygenation is important - Both hypoxia and hypercarbia are to be prevented because they can contribute to secondary neuronal injury (Lewis et al., 2011).
    2. Oxygen administration, artificial airway insertion, intubation, and mechanical ventilation may be required (Lewis et al., 2011).
  3. Neurological Assessment
    1. Glasgow Coma Scale to address LOC, orientation, motor, pupils, speech.language, vital signs, and blood glucose (RNAO, 2005).
  4. Fluid and electrolytes
    1. keep the patient adequately hydrated to promote perfusion and decrease further brain injury (Lewis et al., 2011).
    2. Adequate fluid intake during acute care via oral, IV, or tube feedings should be 1500 to 2000 mL/day (Lewis et al., 2011).
    3. IV solutions and water ware avoided because they are hypotonic and may further increase cerebral edema and ICP(Lewis et al., 2011).
    4. Hyperglycemia may be associated with further brain damage and should be treated (Lewis et al., 2011).
  5. Management of Increased ICP
    1. Improve venous drainage (i.e. elevate HOB)
    2. Maintain head and neck in alignment (Lewis et al., 2011).
    3. Quiet environments will reduce headaches and reduce aggravation of increased ICP (Ignatavicius & Workman, 2013).
    4. 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).
    5. Avoid clustering nursing procedures all at once because the effect of ICP elevation is more dramatic (Ignatavicius & Workman, 2013).
    6. CSF drainage (Ignatavicius & Workman, 2013).
    7. Diuretic drugs (e.g. mannitol, furosemide) (Lewis et al., 2011).
    8. Removal of bone flap to allow for cerebral edema without increases in ICP (Lewis et al., 2011).
  6. Management of Constipation
    1. Constipation can be caused from decreased mobility (Kasaeaneni & Hayes, 2014).
    2. 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).
    3. Fiber supplements such as bran, psyllium, or methylcellulose can be added to help increase the fiber consumed by the patient (Kasaeaneni & Hayes, 2014).
    4. Encourage fluid intakes (Kasaeaneni & Hayes, 2014).
  7. Avoid Hyperthermia
    1. 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).
    2. Treatment: Aspirin Acetaminophen Cool blankets (Lewis et al., 2011).
  8. Education
    1. Teach patients to recognize the symptoms of a stroke by using the acronym FAST
    2. Return demonstrations assist in evaluating family' ability to perform patient care tasks; provide verbal and oral instruction Ignatavicius & Workman, 2013).
    3. Teach family about depression that can occur within 3 months of a stroke. Post stroke depression is associated with increased morbidity (Ignatavicius & Workman, 2013).
    4. Health teaching for the patient includes drug therapy, ambulation skills, nutritional management, and self management skills (Ignatavicius & Workman, 2013).
    5. Health Care Resources (Ignatavicius & Workman, 2013)
      1. Available online resources to share with patients and family include American Heart Association, National Stroke Association, Agency of Health care Research and Quality
2. SLP (Speech Language Pathologist)
  1. Appointments for outpatients speech may be arranged to help the patient relearn to talk (Ignatavicius & Workman, 2013).
  2. 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).
3. Home
  1. Collaborate with case manager to plan patient's discharge; coordinate with rehabilitation therapist to identify need of assistive devices (Ignatavicius & Workman, 2013).
    1. PT (Physiotherapist)
      1. 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).
    2. OT (Occupational Therapist)
      1. To relearn basic skills such as bathing and dressing
4. Community Care
  1. 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).
Complications
1. Increase ICP
  1. Occurs in response to cerebral edema (American Heart Association, 2015).
2. Pneumonia
  1. Due to decreased mobility after a stroke (American Heart Association, 2015).
  2. Aspiration pneumonia
    1. Can be caused by impaired tongue movement, decreased swallowing, or absent gag reflex (American Heart Association, 2015).
3. Urinary Tract Infection
  1. Caused by foley catheter being placed due to bladder incontinence (American Heart Association, 2015).
4. Seizure
  1. Abnormal electrical activity in the brain causing convulsions from cerebral damage (American Heart Association, 2015).
5. Clinical depression
  1. Causes unwanted emotional and physical reactions to changes and losses (American Heart Association, 2015).
6. Pressure ulcers
  1. Results from decreased ability to move and pressure on areas of the body because of immobility (American Heart Association, 2015).
7. Limb contractures
  1. Shortened muscles in an arm or leg from reduced ability to move the affected limb or lack of exercise (American Heart Association, 2015).
8. Deep Vein Thrombosis
  1. Blood clots form in veins of the legs because of immobility from stroke. (American Heart Association, 2015).

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Ischemic Stroke

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