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2010-03-25 20:58:12

Med Surge Stroke/ CVA
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  1. Stroke/ CVA
    • 1.Ischemic insult to
    • brain tissue results in neuron death.

    2.700,000 annually

    • 3rd
    • leading cause of death. Major
    • cause of disability, NH placement
  2. Risk Factors
    • 1.Increase risk with
    • age.

    • 2.AA highest rate. Also increased in Latinos, Native
    • Americans.

    3.Family History
  3. Risk Factors
    • •Smoking
    • •Atrial
    • Fibrillation
    • •Diabetes
    • •Hyperlipidemia
    • •Obesity
    • •Hypercoagulability
    • •OCPs/HRT
    • •Carotid Stenosis
    • •Illicit Drug Use

    • Hypertension most important risk factor.
    • Risk decreases to rate of non-smoker 5 years after quitting.
    • Illicit drugs especially cocaine.
  4. Pathophysiology of Ischemic
    • •Blood flow interrupted to an area of brain
    • results in tissue ischemia.
    • •Ischemia impairs cerebral circulation autoregulation
    • •Ischemic cascade results in release of cytotoxic excitatory amino acids.
    • •Penumbra surrounds area of cell death.
    • Increased CO2 increased cerebral vasodilation and intracranial pressure (ICP

    • 85 % of strokes results from thrombus or embolus. Cell death begins within 5 minutes.
    • Normal cerebral blood vessels dilate or constrict to maintain even flow between MAP of 50-150.
    • Contributes to neuronal cell death.
    • Area of potentially reversible ischemia. Sensitive to change in BP.
  5. Pathophysiology of Ischemic CVA
    • •Blood flow interrupted to an area of brain
    • results in tissue ischemia.
    • •Ischemia impairs cerebral circulation autoregulation
    • •Ischemic cascade results in release of cytotoxic excitatory amino acids.
    • •Penumbra surrounds area of cell death.
    • •Increased CO2 increased cerebral vasodilation and intracranial pressure (ICP)

    • 1.85 % of strokes
    • results from thrombus or embolus. Cell death begins within 5 minutes.
    • 2.Normal cerebral blood
    • vessels dilate or constrict to maintain even flow between MAP of 50-150.
    • 3.Contributes to
    • neuronal cell death.
    • 4.Area of potentially
    • reversible ischemia. Sensitive to
    • change in BP.
  6. Atherosclerosis
    •Endothelial injury

    •Lipid deposits.

    •Lipids calcify over time

    •Platelets, thrombin, and fibrin formation


    •Unstable plaque
  7. Atherosclerosis, cont...
    • 1.Endothelial injury
    • predisposes to lipid deposits and platelet activation.

    • 2.Fatty streaks: the
    • earliest lesions of atherosclerosis: streaks of fat develop in the smooth muscle cells of the blood
    • vessel—turn yellow. Observed by age 15 and increase with age. Believed to be
    • reversible.

    • 3.Platelets release
    • growth factors cause smooth muscle proliferation which further traps lipids.

    • 4.Raised fibrous
    • plaque. Beginning of progressive changes in the arterial wall. Observed by age
    • 30 and increase with age. Initiated by elevated BP, high cholesterol, heredity,
    • carbon monoxide damage due to smoking, immune reactions. In the person with
    • CAD, the endothelium is not rapidly replaced, lipids adhere to damaged blood
    • vessel wall and gradually increases in size. Calcify over time. Platelets
    • accumulate at the site in large numbers which lead to thrombus formation.

    • 5.Complicated lesion
    • stage—plaque consists of core of lipid materials (mainly
    • cholesterol)---continues to grow in size as more lipids and platelets adhere.
    • Lesion hardens causing more damage to arterial wall and may eventually produce
    • narrowing or total occlusion of the artery.

    • 6.Plaque ruptures and
    • can precipitate MI

    • 7.Attributes to two
    • factors: Arterial branching due to chronic ischemia or inherited predisposition
    • to develop new blood vessels—when occlusion of artery happens slowly over a
    • period of time there is a greater chance of collateral circulation developing
    • and myocardium receiving the adequate amount of O2—if it is rapid there is not
    • a chance for collateral circulation to develop—myocardium does not get ample
    • amount of O2 which results in severe ischemia or infarction.
  8. Types of Ischemic Strokes
    • •Thrombotic (61%)
    • –Plaque
    • ruptures and thrombus occludes vessel.
    • –Often
    • preceded by TIA
    • –Usually
    • cardiac source
    • •Atrial
    • Fibrillation
    • •Valve
    • Disease
    • •MI
    • •Endocarditis
    • •Rheumatic
    • Fever

    •Embolic (24%)
  9. Transient Ischemic Attack (TIA)
    •Reversible cerebral ischemia.

    •Deficits resolve within 24 hours.

    •Sign of impending CVA.
  10. Clinical Presentation
    • •Amaurosis Fugax
    • •Weakness, Numbness
    • •Aphasia
    • •Visual Field Cuts.
    • •Diplopia
    • •Vertigo
    • •Ataxia
    • •Syncope
    • •Reflex Asymmetry
    • •+ Babinski
  11. Differential Diagnosis
    • •Migraine
    • •Partial Seizures
    • •Subdural Hematoma
    • •Brain Tumor
    • •Cardiac Syncope
    • •Hypoglycemia
    • •Demyelinating
    • Disease
    • •Encephalitis
  12. TIA = Medical Emergency
    • •Maintain ABCs.
    • •R/O CVA.
    • •Emergent CT to R/O Bleed.
    • •Consider t-PA for Ischemic Stroke within 3 hours of onset.
    • •Avoid aggressive lowering of BP.
    • •Consider in-patient work-up even if symptoms
    • resolve.
  13. Lacunar Stroke
    •Small area of infarct.

    •Penetrating vessel.

    •May be asymptomatic.

    •May contribute to dementia.
  14. Hemorrhagic Stroke
    • •Younger patient.
    • •More severe/worse prognosis
    • •15 % of strokes.
    • •Precipitated by hypertension, aneurysms, arteriovenous malformations (AVM), trauma, tumor, coagulopathy.
    • •Intracerebral bleed: Bleed into brain itself.
    • •Subarachnoid hemorrhage: Bleed between dura and pia mater where CSF flows.
  15. Arterio-Venous Malformation (AVM)
  16. Intracerebral Bleed
    •Sudden onset.

    •Severe headache.


    •Change in mental status.

    •Decreased level of consciousness (LOC).

    •Elevated BP
  17. Subarachnoid Hemorrhage
    •“Worst headache of my life.”

    •Decreased LOC.


    •Focal neurological deficits.

    • •Possible surgery to clip or coil aneurysm or
    • correct AVM.

    •Post-op given nimodipine (Nimotop®) to prevent vasospasm.

    In SAH lysis of subarachnoid clots release metabolites that cause cerebral vasoconstriction and worsen perfusion.
  18. Acute Care of Stroke
    • •“Brain Attack”.
    • •ABC’s
    • •Access EMS and establish time of onset.
    • •Monitor V/S and O2 sat.
    • •Accu-check.
    • •IV access.
    • •Prepare for stat CT.
    • •Seizure Precautions.
    • •Obtain baseline labs

    Baseline labs include CBC, CMP, PT, PTT, cardiac enzymes
  19. Assessment
    • •Neurological
    • –LOC
    • –Glasgow
    • Coma Scale (GCS)
    • –Cranial
    • Nerves
    • –Pupils
    • –Motor
    • –Sensory
    • –DTRs
    • –Cerebellar
    • –NIH
    • Stroke Scale
    • •Cardiac
    • •Respiratory
  20. Nursing Management
    • •Maintain BP.
    • •Maintain fluid balance.
    • •Avoid hypotonic IV solutions.
    • •Control fever.
    • •Limit increases in ICP.
    • •Control Blood Glucose
    • •Screen for Dysphagia

    1.Do not lower unless SBP >220 or MAP 130.

    2.Prevent dehydration or overhydration.

    3.Increase cerebral edema.

    4.Increases metabolic demands of brain.

    5.HOB > 30 degrees, neck in alignment, avoid hip or knee flexion.
  21. tPA Protocol
    • •Must be initiated within 3 to 4.5 hours.
    • –Limited use from 3-4.5 hours (containdicated if age > 80, on anticoagulants, diabetics or prior stroke) (AHA, 2009)
    • •Contraindications:
    • –Rapidly improving symptoms.
    • –Bleed on CT.
    • –Major surgery or trauma within 14 days.
    • –History of GI or GU bleed within 21 days.
    • –Recent arterial puncture at noncompressible site.
    • –SBP> 185 or DBP>110
    • –Coagulopathy (low platelets, elevated PT or aPTT)
    • –History of intracranial bleed.
    • –Recent LP
    • –Seizure at onset of symptoms.
    • –Blood glucose <50 or >400.

    1.Cannot be given if patient wakes up with symptoms.
  22. tPA Nursing Care
    • •Rapidly initiate protocol for appropriate patient.
    • –Assess patient and obtain history.
    • –Stat neuro consult.
    • –Stat labs.
    • –Stat CT.
    • •Closely monitor BP.
    • •Once tPA is initiated monitor closely for
    • neurological status, BP and signs or symptoms of bleeding.
    • •No aspirin, heparin or warfarin for 24 hours.
  23. Diagnostic Tests
    • •Non-Contrast CT
    • 1.R/O bleed. Ischemia may not show rightaway.
    • •MRI
    • 1.Better detail on area of damage.
    • •MRA (Magnetic Resonance Angiography)
    • 1.Non-invasive evaluation of cerebral circulation.
    • •Cerebral Angiogram.
    • Invasive. Risk of vasospasm, embolization, dye reaction. Informed consent.
    • •Carotid Duplex.
    • R/o MI, arrhythmia.
    • •EKG
    • Echocardiogram (TEE) Look for source of
    • emboli.

  24. Treatment of Ischemic Stroke
    • Heparin drip
    • Monitor aPTT 1.5-2.5 control

    • Antiplatelets
    • ASA, Plavix or Aggrenox

    • Warfarin (Coumadin®) for atrial fibrillation
    • Maintain INR 2-3

    •Carotid Endarterectomy.

    –For stenosis > 70%

    • –Risks include stroke, hematoma, infection,
    • nerve injury

    •Carotid Stenting

    •MERCI retriever

    Involves femoral or brachial artery puncture
  25. Post CEA or Carotid Stenting
    •Post-op Monitoring


    • –Neuro
    • Assessment

    • –Neck
    • site

    • –Puncture
    • site
  26. Prevention
    •Risk factor modification:

    • –Control
    • of hypertension.

    • –Smoking
    • cessation.


    • –Healthy
    • diet.

    • –Diabetic
    • control.

    • –Weight
    • loss.

  27. Hazards of Immobility


    •Skin breakdown.




    Shoulder Subluxation
  28. Motor Deficits
    •Depend on area of damage.

    •Contralateral hemiparesis or hemiplegia.

    • •May be arm or leg predominate depending on
    • affected artery.

    •Initial flaccidity and hypoactive reflexes.

    •Eventually spacticity and hyperactive reflexes.
  29. Speech Deficits
    •Usually result from left CVA.

    •Broca’s area = expressive aphasia.

    •Wernicke’s area = receptive aphasia.

    •Aphasia can be non-fluent or fluent.

    •Can have global aphasia.
  30. Emotional Symptoms


  31. Spatial-Perceptual Deficits
    • •Neglect of affected side.
    • •Neglect of sensory input from affected side.
    • •Homonymous Hemianopsia.
    • •Agnosia
    • •Apraxia

    • 1.Denial of deficits.
    • 2.Do not see or hear stimuli from affected side.
    • 3.Blindness on affected side of both eyes.
    • 4.Inability to recognize familiar objects.
    • 5.Inability to carry out learned activities
  32. Homonymous Hemianopsia
  33. Right Sided CVA
    •Left hemiparesis/hemiplegia.

    •Left sided neglect.

    •Prominent spatial-perceptual deficits.



    •Poor safety awareness.

    Impaired judgment.
  34. Left Sided CVA
    •Right hemiparesis or hemiplegia.

    •Language deficits/aphasia.

    •Slow/ cautious behavior.

    •Aware of deficits.


    •Impaired comprehension.
  35. Left CVA
  36. Nursing Care for Mobility
    •Maintain ROM.

    •Position to prevent contractures.

    •Prevent foot drop.

    •Fall precautions.

    •Transfer to strong side.

    •Address functional incontinence.
  37. Nursing Care for Aphasia
    •Assess communication deficit.

    •Eliminate distractions.

    •Ask yes or no questions.

    •Communicate 1 thought at a time.

    •Use demonstrations or gestures.

    •Give patient time to respond.

    •Be patient.
  38. Nursing Care for Unilateral Neglect
    •Place objects in patient’s visual field.

    •Approach patient from unaffected side.

    •Teach patient to turn head to affected side.

    •Teach patient to stimulate affected side.

    • •Teach patient to use mirror to survey
    • affected side.
  39. Nursing Care for Emotional Lability
    •Provide emotional support.

    •Explain behavior to family.

    •Maintain a calm environment.
  40. Nursing care for Dysphagia
    •Assess gag reflex.

    •Assess swallowing function.

    •Screen all stroke patients.

    •Initiate speech consult.

    •Check for pocketing.

    •Modified consistency diet.

    •Sit up to 90 degrees.

    •Chin tuck.

    •Double swallow.

    •Tube feed if aspirating.
  41. Collaborative Care
    •Physical Therapy (PT): Mobility, gait, transfer, strengthening.

    • •Occupational Therapy (OT): ADL, coping with
    • cognitive and perceptual deficits.
    • Adaptive equipment.

    •Speech Therapy: Evaluation and treatment of aphasia, dysarthria, dysphagia.
  42. Damage to which part of the brain is
    responsible for expressive aphasia?
    Answer Unknown

    • –A)
    • Wernicke’s area

    • –B)
    • Broca’s Area

    • –C)
    • Parietal lobe

    • –D)
    • None of the above
  43. •Which of the following patients is at higher
    risk for falls?
    Answer Unknown

    • –A)
    • Left brain CVA

    • –B)
    • Right Brain CVA

    • –C)
    • Both Equally at risk
  44. John Smith is an 85 year old male who began
    experiencing right sided weakness and difficulty speaking 30 minutes ago. His BP is 160/90. He is not on anticoagulants. Which of the following are true:
    Answer Unknown

    • –A)
    • He is a candidate for tPa.

    • –B)
    • He is not a candidate for tPa

    • –C)
    • He needs a CT and thorough history to determine eligibility for tPa

    • –D)
    • He is too old to receive tPa