Cerebrovascular Disorders

Cerebrovascular Disorders

Functional abnormality of the CNS Occurs: normal blood supply to brain is disrupted

Stroke: Stats & Incidence

Primary cerebrovascular disorder; third leading cause of death in the U.S. Leading cause of serious long-term disability in the U.S. 700,000 strokes (U.S.); 500,000: new strokes; 200,000: recurrent 3/4 occur in people over age 65; risk doubles each decade after age 65 25% survive initial stroke: die within 1st yr.

Can occur at any age; occur under age 65

Financial impact: 57 million (ADA, 2005)
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Major Stroke Categories

Ischemic (85%)

Embolic or thrombotic

Hemorrhagic (15%)

Risk Factors

Nonmodifiable risk factors

Age (over 55), male gender, African American race

Hypertension: the primary risk factor-Controlling HTN is key to preventing stroke

Modifiable risk factors: see Chart 62-1

Cardiovascular disease: asymptomatic carotid stenosis, valvular heart disease; a-fib

Elevated cholesterol or elevated hematocrit Obesity

Diabetes
Oral contraceptive use Smoking, drug and alcohol abuse
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Ischemic Stroke

Cerebrovascular accident (CVA) or brain attack Sudden loss of function resulting from disruption of the blood supply to a part of the brain. Subdivided in 5 different types based on cause
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Types of Ischemic Strokes

Large artery thrombotic stroke

Atherosclerotic plaque Thrombus formation & occlusion = ischemia &

infarction

Small penetrating artery thrombotic stroke Cardiogenic embolic strokes Cryptogenic strokes Other
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Anatomy of Cerebral Circulation

Blood is supplied to the brain by two major pairs of arteries

Internal carotid arteries (ant. Circulation) Vertebral arteries (post. Circulation) Frontal, parietal, and temporal lobes Basal ganglia Part of the diencephalon

Carotid arteries branch to supply most of the

Thalamus Hypothalamus
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Cerebral Circulation

The brain comprises only 2% of the body's weight but receives 20% of the blood supply. Over 150,000 people have strokes each year, largely resulting from blockages in the arteries and veins. Unimpeded circulation of blood to and from the brain is critical to health.

Anatomy of Cerebral Circulation

Vertebral arteries join to form the basilar artery, which supply the

Middle and lower temporal lobes Occipital lobes Cerebellum Brainstem Part of the diencephalon
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Regulation of Cerebral Blood Flow

Blood flow: maintained at 20% of CO for optimal brain functioning. Total interruption of blood flow:

neurological metabolism altered in 30 seconds; metabolism stops in 2 minutes; cellular death occurs in 5 minutes

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Regulation of Cerebral Blood Flow.

Brain is normally well protected from changes in mean systemic arterial blood pressure by a mechanism known as

cerebral autoregulation.

Cerebral autoregulation involves:

Changes in the diameter of cerebral blood vessels in response to changes in pressure so that the blood flow to the brain stays constant
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Regulation of Cerebral Blood Flow.

Factors that affect blood flow to the brain

Systemic blood pressure Cardiac output Blood viscosity

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Regulation of Cerebral Blood Flow

Collateral circulation may develop to compensate for a decrease in cerebral blood flow An area of the brain can potentially receive blood supply from another blood vessel if its original blood supply is cut off.

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Cerebral arteries & Circle of Willis

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Regulation of Cerebral Blood Flow

Atherosclerosis: a major cause of stroke Can lead to thrombus formation and contribute to emboli

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Pathophysiology: Ischemic Stroke

Disruption of the cerebral blood flow from an obstructed or occluded vessel Ischemic cascade

Decrease of cerebral blood flow to < 25 mL/100 g/minute Energy failure: neurons no longer able to maintain aerobic respiration Acidosis: result of large amt. of lactic acid causing a change in the pH level Ion imbalance: membrane pump begins to fail & cells cease to function
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Pathophysiology: Ischemic Stroke.

Ischemic cascade (cont.)

Early: penumbra region around area of infarct Glutamate: depolariztion of the cell wall leading to increase in intracellular calcium and
release of glutamate

Cell membrane destruction, protein breakdown, vasoconstriction, free radical formation = enlarge area of infarct into penumbra, extending the stroke Cell injury and death
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Transient Ischemic Attack

TIA, mini-stroke Temporary focal loss of neurologic function caused by ischemia Lasts <24 hrs & often lasts <15 min. Most resolve: within 3 hours Due to microemboli that temporarily block blood flow Warning signs of progressive cerebrovascular disease

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Clinical Manifestations

Carotid system involvement Temporary loss of vision in one eye Transient hemiparesis Numbness or loss of sensation Sudden inability to speak

Vertebrobasilar system Tinnitus Vertigo Darkened or blurred vision Ptosis Dysphagia Ataxia Unilateral or bilateral numbness 21 or weakness

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Assessment/Dx/Management

Ct Scan w/without contrast Cardiac monitoring & testing Drugs that prevent platelet aggregation Anticoagulation therapy

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Ischemic Stroke

Inadequate blood flow to the brain from partial or complete occlusion of an artery Further divided into thrombotic & embolic

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Ischemic Stroke

Thrombotic

Injury to a blood vessel & formation of a blood clot Thrombotic stroke: result of thrombosis or narrowing of a blood vessel: most common cause of stroke: 60% Gender: _______________ Warning: ____________________ Time of onset: ________________________ Course/Prognosis: ________________________ _______________________________________
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Ischemic Stroke..

Embolic Occlusion of cerebral artery from the lodging of an embolus = infarction & edema of area 2nd most common cause of stroke (24%) Majority emboli: originate in endocardial (inside) layer of the heart Rapid occurrence of clinical symptoms

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Ischemic Stroke:

Embolic (cont.)

Gender: _____________ Warning: ____________ Time of onset: _______________ Course/Prognosis: ______________________ _____________________________________ _____________________________________

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Clinical Manifestations

General s/s Numbness or weakness: face, arm or leg e specially on one side of the body-Major presentationIschemic stroke Confusion or change in MS Trouble speaking or understanding speech Visual disturbances Loss of balance, dizziness Difficulty walking Sudden severe headache
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Clinical Manifestations: Motor Loss

Hemiplegia: most common motor dysfunciton, Hemiparesis Early stage: Flaccid paralysis & loss or decrease in DTR (INITIAL clinical feature) Abnormal increased muscle tone (spasticity): After 48 hours
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COMPARISON OF LEFT AND RIGHT HEMISPHERIC STROKES

Left Hemispheric Stroke

Right Hemispheric Stroke

Paralysis or weakness on right side of body of body Right visual eld decit Aphasia (expressive, receptive, or global) Altered intellectual ability Slow, cautious behavior

Paralysis or weakness on left side of body Left visual eld decit Spatial-perceptual decits Increased distractibility Altered intellectual ability Impulsive behavior and poor judgment Lack of awareness of decits

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Communication Loss

Language & communication disturbance Stroke: most common cause of aphasia

Dysarthria Dysphagia or aphasia

Expressive aphasia (L frontal damage) Receptive aphasia (temporal lobe damage) Global aphasia (mixed)
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Apraxia

Perceptual Disturbance

Ability to understand sensation Disturbances can result in: Visual-perceptual: disturbance of primary sensory pathways b/w eye & visual cortex

Homonymous Hemianopsia (loss of half of the visual field)

Perceiving the relationship of two or more objects in spatial areas Frequently seen in patients with R hemispheric damage
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Visual-spatial relations

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Sensory Loss

May take form of impairment of touch More severe: loss of prioprioception (inability to perceive the position and motion of body parts) Difficulty interpreting visual, tactile and auditory stimuli. Agnosias (deficits in the ability to recognize previously familiar objects perceived by one or more of the senses.
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Cognitive Impairment & Psychological Effects

Frontal lobe damage:

Learning capacity, memory or other higher cortical intellectual functions are impaired Dysfunctions reflected in a limited attention span, difficulty w/comprehension, forgetfulness, lack of motivation Common Other: emotional lability; frustration, resentment, lack of cooperation, as well as other psychological issues
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Depression:

Assessment/Dx

Complete H&P, neurologic exam Initial assessment: focuses on: airway patency; Cardiovascular status: BP, cardiac rhythm, rate, carotid bruit; gross neurologic deficits Initial dx test: Ct Scan: noncontrast 12-lead EKG Carotid u/s, dopplers Cerebral angiography Transcranial doppler, MRI of brain, neck or both Xenon-CT scan, Singple photon emission (SPECT) scan, PET scan
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Assessment/Dx..

Additional studies

Complete blood count Platelets, prothrombin time, activated partial thromboplastin time Electrolytes, blood glucose Renal and hepatic studies Lipid profile

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Prevention

Primary prevention: best approach Stroke screenings Help patients alter risk factors for stroke Prepare & support pt through carotid endarectomy Administer anticoagulant agents: low-dose ASA Rx); Coumadin (if a-fib)
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Medical Managment

Afib: Coumadin: unless contraindicated. INR:

target 2.5

ASA: best option if coumadin contraindicated Platelet-inhibiting medications

Plavix, Persantine, Ticlid (rarely used)

Statins: simvastatin (Zocor) Antihypertensive meds: after acute stroke period: Ace inhibitors & thiazide diuretics
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Thrombolytic Therapy

Dissolve blood clot Recombinat t-PA

Binds to fibrin and converts plaminogen to plasmin, which stimulates fibrinolysis of the atherosclerotic lesion

Rapid dx of stroke and initiation of thrombolytic therapy (within 3 hours) with ischemic stroke
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Enhancing Prompt Dx

Upon immediate notification: Stroke team awaits pts arrival Initial mgmt: CT Scan, determination of pt meeting criteria for t-PA Once pt meets t-PA criteria: No anticoagulant given for next 24 hrs

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Dosage & Administration

Weight-based Dosage: 0.9 mg/kg, max. dose of 90 mg 10% calculated dose: adm. IV bolus over 1 minute; remaining given IV over 1 hour via infusion pump Vital signs- obtained frequently, with particular attention to blood pressure Goal of lowering the risk of intracranial hemorrhage).

Blood pressure should be maintained with the systolic pressure less than 180 mm Hg and the diastolic pressure less than 105 mm Hg Airway management is instituted based on the patients clinical condition
and arterial blood gas values.
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Side Effects

BLEEDING: most common Intracranial bleeding (major complication)

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Other

Requires ICU or acute stroke unit setting Airway assessment Continous cardiac assessment/monitoring Frequent neuro assessment Frequent vs. esp. BP: goal of lowering IC hemorrhage) BP: maintain SBP <180 and DBP < 105 ABG
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Therapy for Pts w/Ischemic Not Receiving t-PA

Anticoagulation Rx: IV Heparin, low-molecular weight heparin Maintenance of cerebral hemodynamics Administration of osmotic diuretics: mannitol Maintaining PaCO2 with range of 30-35 mm Hg Positioning to avoid hypoxia HOB elevated to promote venous drainage to lower increased ICP Intubation to establish patent airway, if necessary Maintain CO 4-8 L/min
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Managing Potential Complications

Cerebral hypoxia: give supplemental O2 Decreased cerebral blood flow & extension of the area of injury: hydraton and avoid HTN or hypotension, maintain airway, give O2 Monitor for UTI, cardiac abnormalities, immobility
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Surgical Prevention

Carotid Endarectomy

Removal of an atherosclerotic plaqued or thrombus from carotid artery to prevent stroke in patients with occlusive disease of the extracranial cerebral arteries.

Indicated for symptoms of TIA or mild stroke found to be caused by severe:

70-90% carotid artery stenosis Moderate stenosis (50-69%) with other significant risk factor
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Carotid Endarterectomy

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Carotid Stenting

Less invasive Used for severe stenosis Selected pts who are high risk for surgery

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Medical ManagementAcute Phase of Stroke

Prompt diagnosis and treatment Assessment of stroke: NIHSS assessment tool Thrombolytic therapy Criteria for tPA IV dosage and administration Patient monitoring Side effectspotential bleeding Elevate HOB unless contraindicated Maintain airway and ventilation Continuous hemodynamic monitoring and neurologic assessment

Nursing Process: The Patient Recovering from an Ischemic StrokeAssessment

Acute phase
Ongoing/frequent monitoring of all systems including vital signs and neurologic assessmentLOC, motor symptoms, speech, eye symptoms Monitor for potential complications including musculoskeletal problems, swallowing difficulties, respiratory problems, and signs and symptoms of increased ICP and meningeal irritation After the stroke is complete Focus on patient function; self-care ability, coping, and teaching needs to facilitate rehabilitation

Assessment

Acute phase Neuro assessment & document on flow sheet

Change in LOC or responsiveness Presence of absence of voluntary or involuntary movements of extremities; muscle tone, body posture and position of head Eye opening Stiffness of neck 53 See notes below**

Nursing Process: The Patient Recovering from an Ischemic StrokeDiagnoses

Impaired physical mobility Acute pain Self-care deficits Disturbed sensory perception Impaired swallowing Urinary incontinence Disturbed thought processes Impaired verbal communication Risk for impaired skin integrity Interrupted family processes Sexual dysfunction

Nursing Process: The Patient Recovering from an Ischemic StrokePlanning

Major goals 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 Absence of complications

Nursing Management

Primary complication: CE: Stroke, CN injuries, infection or hematoma at incision & carotid artery disruption Maintain BP in immediate postop phase Avoid hypotension: To prevent cerebral ischemia and thrombosis Sodium nitroprusside: to reduce BP Close cardiac monitoring
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Nursing Management

Post:

Neuro assessments & record; notify surgeon if deficit occurs Monitor CN involvement: difficulty swallowing, hoarseness or other signs Focus assessment of CN: CN: ________________ CN:_________________ CN: ________________ CN:_________________ Edema: expected postop; extensive edema and hematoma: obstruct airway Emergency airway supplies: _______________

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Interventions

Focus on the whole person

Provide interventions to prevent complications and to promote rehabilitation Provide support and encouragement Listen to the patient
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Improving Mobility and Preventing Joint Deformities

Turn and position the patient in correct alignment every 2 hours

Use splints Practice passive or active ROM 4 to 5 times day Position hands and fingers Prevent flexion contractures; Prevent shoulder abduction Do not lift by flaccid shoulder Implement measures: prevent and treat shoulder 59 problems

Positioning to Prevent Shoulder Abduction

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Prone Positioning to Help Prevent Hip Flexion

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Improving Mobility and Preventing Joint Deformities

Perform passive or active ROM 4 to 5 times day Encourage patient to exercise unaffected side Establish regular exercise routine Use quadriceps setting and gluteal exercises Assist patient out of bed as soon as possible: assess and help patient achieve balance and move slowly Implement ambulation training
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Interventions

Enhance self-care

Set realistic goals with the patient

Encourage personal hygiene Ensure that patient does not neglect the affected side Use assistive devices and modification of clothing

Provide support and encouragement Implement strategies to enhance communication: see Chart 62-4 Encourage the patient with visual field loss to turn his head and look to side
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Interventions

Nutrition

Consult with speech therapist or nutritionist

Have patient sit upright to eat, preferably OOB Use chin tuck or swallowing method Feed thickened liquids or pureed diet Assess and schedule voiding

Bowel and bladder control

Implement measures to prevent constipation: fiber, fluid, and toileting schedule Provide bowel and bladder retraining
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Interventions.

Improve thought processes Maintain skin integrity Improve family coping Help patient cope with sexual dysfunction Promote home and community-based care
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Charts: Review

62-3: Assistive devices to Enhance Self-care after Stroke 62-4: Communicating with the Patient with aphasia

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Hemorrhagic Stroke

Primarily caused by: intracranial or subarachnoid hemorrhage Bleeding into brain tissue, ventricles or subarachnoid space Primary: Spontaneous rupture of small vessels (80%) primarily related to uncontrolled hypertension; Subarachnoid hemorrhage due to a ruptured aneurysm;

Secondary

intracerebral hemorrhage related to amyloid angiopathy, arterial venous malformations (AVMs), intracranial aneurysms, neoplasm or medications such as anticoagulants, amphetamines.

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Pathophysiology

Aneurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space) Normal brain metabolism disrupted from entry of blood into subarachnoid space

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Intracerebral hemorrhage

Bleeding into brain substance Most common in pts: HTN & cerebral atherosclerois Bleeding: most common in cerebral lobes, basal ganglia, thalamus, brain stem (pons), & cerebellum Bleeding ruptures wall of lateral ventricle leading to intraventricular hemorrhage: fatal
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Intracranial (Cerebral) Aneurysm

Dilation of the walls of a cerebral artery Develops as a result of a weakness in arterial wall Cause: unknown Lesions occur: bifurcations of large arteries at circle of Willis Cerebral arteries most commonly affected: ICA (internal carotid), ACA ( anterior carotid), ACoA (anterior communicating artery), PCoA (post. Communicating artery), PCA (post. Cerebral artery), MCA (middle cerebral artery)
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Arteriovenous Malformations

AVM Due to an abnormality in embryonic development that leads to a tangle of arteries and veins in brain that lacks a capillary bed Absence of capillary bed leads to dilation of arteries and veins & eventual rupturee Common cause of hemorrhagic stroke: young people
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Intracranial Aneurysms

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Subarachnoid Hemorrhage

Hemorrhage into subarachnoid space Occurs as a result of AVM, intracranial aneurysm, trauma or HTN Most common causes

Leaking aneurysm in area of circle of Willis Congential AVM of the brain

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Clinical Manifestations

Conscious pt: Severe headache Neurologic deficits: motor, sensory, cranial nerve, cognitive Other: vomiting Early: sudden change in LOC Possible focal seizures (brain stem involvement)
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Clinical Manifestations

Unique s/s besides those similar to ischemic

Aneurysm rupture or AVM: sudden, unsually severe headache, often LOC for a variable period of time Pain, rigidity in back of neck (nuchal rigidity) & spine due to meningeal irritation Visual disturbance: loss, diplopia, ptosis: aneurysm near oculomotor nerve Tinnitus, dizziness, hemiparesis
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Assessment/Dx

CT Scan: type of stroke, size, location of hematoma, presence or absence of ventricular blood & hydrocephalus. Cerebral angiography: confirms dx of IC aneurysm or AVM Lumbar puncture: if evidence of ICP Drug Toxicology screen: dx hemorrhagic stroke in pt under age 40 Hunt-Hess classification system: guides physician in dx severity of subarachnoid hemorrhage after an aneurysmal bleed (see Chart 62-6)
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Prevention

Primary prevention: best approach Manage HTN and other risk factors Stroke screenings Increase public awareness regarding association between phenylpropanolamine (PPA), an ingredient in appetite suppresants as well as cold and cough meds
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Complications

Rebleeding Cerebral vasospasm resulting in cerebral ischemia Seizures

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Complications

Acute hydrocephalus: free blood obstructing reabsorption of CSF by arachnoid villi

1st 24 h post subarachnoid hemorrhage or several days [subacute] to weeks [delayed]

Hyponatremia-post subarachnoid hemorrhage

Must check serum Na & report if <135 mEq/L to provider if persistent for 24h or longer Must then evaluate for SIADH or cerebral salt wasting syndrome

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Cerebral Hypoxia & Decreased Blood Flow

Immediate hemorrhagic stroke complications:

Cerebral hypoxia Decreased blood flow Extension of the area of injury

Provide adequate O2 to brain Maintain supplemental O2 Maintain H&H Maintain hydration (IVF): reduce blood viscosity and improve blood flow Avoid extremes of HTN or hypotension Observe for seizure activity
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Vasospasm

Cerebral vasospasm (narrowing of the lumen of the involved cranial blood vessel) Serious complication of subarachnoid hemorrhage and Accounts for 40% to 50% of the morbidity and mortality of those who survive initial IC bleed
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Vasospasm..

Worsening headache, a decrease in level of consciousness (confusion, lethargy, and disorientation), or a new focal neurologic deficit (aphasia, hemiparesis Frequently occurs 4 to 14 days after initial hemorrhage, when the clot undergoes lysis (dissolution) administration of calcium-channel blockers: nimodipine (Nimotop) during the critical period in which vasospasm may occur can prevent delayed ischemic deterioration
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Increased ICP

Often follows a subarachnoid hemorrhage CSF drainage may be instituted by cautious Lumbar puncture or ventricular catheter drainage Mannitol: Used as long-term measure to control ICP: dehydration and disturbances in e-lyte balance (hyponatremia or hypernatremia, hypokalemia or hyperkalemia)
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Systemic HTN

Prevention is critical SBP lowered to less than 150 mmHg to prevent hematoma enlargement Elevated BP: antihypertensive meds:

Labetalol: Normodyne Nicardipine (Cardene) Nitroprusside (Nitro-press

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Systemic HTN

Arterial hemodynamic monitoring: to detect and avoid a precipitous drop in blood pressure, which can produce brain ischemia.

Antiseizure agents are often administered prophylactically.

Stool softeners are used to prevent straining, which can also elevate the blood pressure.
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Medical Management

Allow brain to recover from initial insult Supportive mainly Bedrest, sedation Stress management of vasospasm Surgial or medical tx to prevent rebleeding Anagesics: codeine, acetaminophen: head and neck pain SCDs: prevent DVT
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Surgical Management

Diameter of bleed > 3 cm & GCS decreases Surgical evacuation: most frequently done via a craniotomy Goal: prevent bleeding in an unruptured aneurysm or further bleeding in an already ruptured aneurysm.
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Surgical Interventions

Endovascular procedures Endovascular tx (occlusion of parent artery) Aneurysm coiling (obstruction of the aneurysm site with a coil)
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Postop Complications

Psychological symptoms: disorientation, amnesia, Korsakoffs syndrome, personality changes Intraoperative embolization, postop internal artery occlusion, f/e disturbances from dysfunction of neurohypophyseal system) & GI bleeding
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Nursing Process: The Patient with a Hemorrhagic StrokeAssessment

Complete and ongoing neurologic assessmentuse neurologic flow chart Monitor respiratory status and oxygenation Monitoring of ICP Patients with intracerebral or subarachnoid hemorrhage should be monitored in the ICU Monitor for potential complications Monitor fluid balance and laboratory data All changes must be reported immediately

Nursing Diagnoses Ineffective tissue perfusion (cerebral) Disturbed sensory perception Anxiety

Collaborative Problems/Potential Complications

Vasospasm Seizures Hydrocephalus Rebleeding Hyponatremia

Planning

Goals may include:

Improved cerebral tissue perfusion Relief of sensory and perceptual deprivation Relief of anxiety The absence of complications

Absolute bed rest Elevate HOB 30 to promote venous drainage or flat to increase cerebral perfusion Avoid all activity that may increase ICP or BP; Valsalva maneuver, acute flexion or rotation of neck or head Exhale through mouth when voiding or defecating to decrease strain Nurse provides all personal care and hygiene Nonstimulating, nonstressful environment; dim lighting, no reading, no TV, no radio Prevent constipation Visitors are restricted

Aneurysm Precautions

Home Care and Teaching for the Patient Recovering from a Stroke

Prevention of subsequent strokes, health promotion, and follow-up care Prevention of and signs and symptoms of complications Medication teaching Safety measures Adaptive strategies and use of assistive devices for ADLs Nutritiondiet, swallowing techniques, tube feeding administration Eliminationbowel and bladder programs, catheter use Exercise and activities, recreation and diversion Socialization, support groups, and community resources

Interventions

Optimize cerebral tissue perfusion Relieve sensory deprivation and anxiety Keep sensory stimulation to a minimum for aneurysm precautions Implement reality orientation Provide patient and family teaching Provide support and reassurance Implement seizure precautions Implement strategies to regain and promote self-care and rehabilitation
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Question
What are expected patient outcomes for a patient recovering from a hemorrhagic stroke? A. Exhibits absence of vasospasm B. Residual aphasia C. One to four seizures D. Complains of visual changes

Practice

A nurse is caring for a patient diagnosed with a transient ischemic attack [TIA] is scheduled for a carotid endarterectomy. What rationale for the procedure should the nurse give the patient? a. It will decrease cerebral edema b. It will help prevent seizure activity that is common following a TIA . c. It helps prevents a stroke by removing fatty plaques blocking cerebral flow. d. It will help determine the cause of the mini stroke.
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Practice

What is the earliest sign of decompensation in a patient with a hemorrhagic stroke? a. Headache b. Change in level of consciousness c. Grand mal seizures d. Dyspnea
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Practice

A nurse is caring for a patient diagnosed with a hemorrhagic stroke. What is the priority goal for the patient? a. Maintain urine output greater than 30 mL/hour. b. Maintain and improve cerebral tissue perfusion. c. Relieve anxiety. d. Relieve sensory deprivation.
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Practice

A nurse is caring for a patient with a cerebral aneurysm who suddenly reports a very severe headache. What priority nursing action should the nurse take immediately? a. Sit with the patient for a few minutes. b. Administer an analgesic. c. Inform the nurse-manager. d. Call the physician immediately.
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Practice

Which patient has the highest risk for a stroke? a. White female, age 60, with history of chronic alcohol intake b. White male, age 60, with history of uncontrolled high blood pressure c. Black male, age 60, with history of type 2 diabetes d. Black male, age 50, with history of 20 year smoking history
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Practice

A _________________ is a neurological deficit lasting less than 24 hours, with the most episodes resolving in less than 1 hour. Administration of ______________________ such as Coumadin inhibits clot formation and may prevent both thrombotic and embolic strokes.

Research has shown that the time period of ____________hours is necessary for eligibility of thrombolytic therapy.
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Practice

When positioning a stroke patient, it is recommended that the __________ position be implemented for 15 to 30 minutes several times a day to promote hyperextension of the hip joints and prevent contracture deformities of the shoulders and knees. _______________________is the most common and serious psychological problem in a patient who has had a stroke.

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