Cerebral Vascular Accident

1
Cerebral Vascular Accident

• STROKE

2
(No Transcript)
3
RISK FACTORS FOR STROKES

• Nonmodifiable
• Age- incidence ? with age until age 75.
• Race- higher in African Americans
• Gender- higher in men
• Heredity- family history increases risk

• Potentially Modifiable
• Lifestyle- excessive alcohol, cigarette smoking,
  obesity, high fat diet, drug abuse.
• Pathologic conditions- cardiac disease, DM, HTN,
  migraine headaches, hypercoagulability states.

4
(No Transcript)
5
ETIOLOGY AND PATHO

• Extra-cranial factors- related to the circulatory
  system.
• Systemic blood pressure- lt70 and gt160
• cardiac output- when reduced by 30 cerebral
  blood flow is reduced.
• Blood viscosity- anemia increases cerebral blood
  flow and polycythemia reduces it.

6
INTRACRANIAL FACTORS

• A. Metabolic factors
• Increased CO2 and low O2 results in vasodilation
  to restore blood flow to normal.
• CO2 is the most potent regulator of cerebral
  blood flow.
• Increased Hydrogen ion concentration increases
  cerebral blood flow.

7
Intracranial factors, contd

• B. Blood vessels
• The condition of the blood vessels supplying the
  brain is important!!!
• Potential problems- congenital anomalies
  (tortuosity, coiling, kinking, and AV
  malformations).
• The malformations interfere with cerebral blood
  flow and contribute to atherosclerotic disease
• Collateral circulation develops
• Circle of Willis

8
Intracranial factors, contd

• C. Intracranial pressure
• ICP increases with an assault to brain.
• Causes of ICP stroke, neoplasms, inflammation,
  trauma, and hydrocephalus.
• ICP compresses the brain and reduces cerebral
  blood flow, which may lead to infarct.
• Both extracranial and intracranial factors may
  lead to stroke

9
Atherosclerosis

• An abnormal accumulation and infiltration of in
  the intima of the arteries.
• Plaques develop in an area of high turbulence
  which may later damage the plaque.
• Platelets and fibrin aggregate or collect on the
  surface of the plaque.
• Parts of the plaque breaks off and travel to a
  narrower distal artery
• Cerebral infarct occurs.

10
(No Transcript)
11
(No Transcript)
12
(No Transcript)
13
TYPES OF STROKE

• Ischemic Most common type of stroke!
• Occurs due to decreased blood flow to an area of
  the brain due to partial or complete occlusion of
  and artery due to thrombosis.
• This lack of blood, oxygen and nutrients to an
  area of the brain causes necrosis of cerebral
  tissue.
• Two types thrombotic and embolic
• See Lewis, page 1648 table 55-1.

14
Thrombotic stroke

• Most common cause of cerebral infarct!
• Cause Due to formation of a blood clot or
  coagulation of blood that results in narrowing of
  blood vessel or occlusion.
• 2/3 of strokes due to HTN or DM. (accelerate the
  atherosclerotic process)
• May also be due to oral contraceptives,
  coagulation disorders, polycythemia, arteritis,
  chronic hypoxia and dehydration.

15
(No Transcript)
16
Thrombotic Stroke

• Thrombotic strokes are usually proceeded by
  prodromal episodes (warnings) called TIAs
  (transient ischemic attacks).
• TIAs last from 5 to 30 minutes.
• Include- paresis or decreased strength and motion
  of an extremity.
• Aphasia or disturbance of language function,
• Paralysis, mental confusion, or visual
  disturbances.

17
Thrombotic stroke

• The extent of the stoke depends on rapidity of
  onset, size of lesion, and presence collateral
  circulation.
• There is a pattern to thrombotic stroke!
• 1. single attack symptoms occur over several
  hours
• 2. intermittent progression toward a stroke over
  hours or days.
• 3. partial stroke with permanent neuro deficits
• 4. series of TIAs followed by a stroke with
  permanent neuro deficits.

18
Thrombotic stroke

• Symptoms at 72 hours are usually due to resulting
  edema to tissues symptoms improve after edema
  subsides (_at_ 2 weeks).
• This type of stroke occurs during or after
  stroke.

19
(No Transcript)
20
(No Transcript)
21
EMBOLIC STROKE

• Cerebral embolism results from occlusion of
  cerebral artery by an embolus.
• Necrosis and cerebral edema results.
• Embolus is the second most common cause of
  stroke.
• Most emboli originate in the endocardium with
  plaques or tissue breaking off and entering
  circulation.

22
(No Transcript)
23
Embolic Stroke

• Emboli are associated with heart conditions such
  as
• A fib
• MI
• Infective endocarditis
• Rheumatic heart disease
• Valvular prostheses
• ASD

24
Embolic stroke

• Less common causes of emboli
• Air
• Fat from long bone fracture
• Amniotic fluid postpartum
• tumors

25
Embolic stroke

• Prodromal warning less likely single events
• sudden onset
• Most commonly related to head trauma
• High rate of re-occurrence if cause is not
  treated.

26
Hemorrhagic stroke

• Intracerebral hemorrhage is bleeding within the
  brain caused by rupture of a blood vessel that
  lasts from minutes to days.
• Most commonly caused by HTN
• May be caused by brain tumors, trauma,
  thrombolytic drugs, and ruptured aneurysms.

27
Hemorrhagic stroke

• Blood within the closed area of the brain imposes
  pressure on the brain tissue and displaces brain
  tissue and decreases blood flow to brain.
• Clinical manifestations depends on the site and
  amount of hemorrhage and resultant damage.
• Poor prognosis 70 die

28
(No Transcript)
29
Subarachnoid stroke

• Caused by aneurysms, AV malformations, trauma,
  and HTN.
• May have prodromal symptoms if ballooning or
  dilation applies pressure to brain tissue.
• May suddenly rupture, causing neuro changes
• Majority of aneurysms are in the Circle of Willis

30
Subarachnoid hemorrhage, contd

• If aneurysm leaks, pt may have a headache!
• Rupture of aneurysm causes pressure in
  subarachnoid space due to bleeding. Clinical
  manifestations
• Headache, lethargy, confusion, nausea, vomiting,
  fever, neck pain, and backaches, paralysis, coma
  and death.
• Massive hemorrhage is defines as 30 to 50 ml of
  blood.
• Watch for re-bleeding when clot starts to
  dissolve. (usually within first 2 weeks post
  rupture). Reduce activity and prevent straining.

31
Temporal Development of CVA

• Transient Ischemic Attacks (TIAs)-
• Brief episodes of neuro manifestations (less than
  24 hours).
• Leaves no residual effects
• Three categories
• 1/3 never have another TIA
• 1/3 will have more than one TIA
• 1/3 will have a stroke
• WARNING SIGNS OF PROGRESSING CVA!

32
TIAs

• s/s vary depending on the part of brain affected.
• Treatment
• Medications such as aspirin, Persantine
  (dipyridamole), Ticlid, and anticoagulant
  medication.
• Long term therapy post TIA
• Surgical treatment- carotid endartarectomy,
  extra-cranial- intracranial bypass (EC-IC
  bypass), and transiluminal angioplasty.

33
Reversible ischemic Neurologic Deficit

• A neuro deficit which remains 24 hours after
  onset but leaves no residual signs or symptoms.
• Considered a completed stroke with minimal to no
  residual deficits

34
Stroke In- Evolution

• A progressive stroke which develops over hours
  or days.
• Characteristic of an enlarging intra-arterial
  thrombus.
• A stepwise or intermittent progression of
  deterioration of neurological symptoms.
• Manifestations do not resolve and leave residual
  damage.

35
Completed Stroke

• Neuro defects unchanged over 2 to 3 days.
• Usually embolic in nature
• Also called stable stroke.
• Signals readiness for aggressive rehab therapy.
  (unless an aneurysm is involved).

36
Clinical Manifestations

• All deficits are directly related to area of
  brain that is involved.
• See Lewis, page 1650, Table 55-2.

37
Neuromotor Function

• Destruction of motor neurons in the pyramidal
  pathway causes
• Mobility
• Respiratory function
• Swallowing and speech
• Gag reflex
• Self-care abilities

38
Motor deficits

• Loss of skilled voluntary movement (akinesia).
• Impairment of integration of movements
• Alterations in muscle tones
• Alteration in reflexes
• Initial hypo-reflexia which progresses to
  hyper-reflexia for most patients.

39
Patterns of deficits

• Contralateral deficits
• A lesion on one side of the brain affects the
  motor function on the other side of the brain.
• The arms and legs on the affected side may be
  weak or paralyzed to different degrees depending
  the degree of cerebral circulation compromised.
• See Lewis, Page 1651 Table 55-5

40

• The affected shoulder tends to rotate internally
  the hip rotates externally.
• The affected foot is plantar flexed and inverted.
• An initial period of flaccidity may lasts for
  several days to weeks.
• Spasticity of muscles follows the flaccid stage
  and is related to interruption of upper neuron
  influence.

41
Communication

• Aphasia- total loss of comprehension and use of
  language due to damage to the dominant hemisphere
  (left hemisphere).
• Dysphasia-dysfunction related to comprehension or
  use of language due to partial disruption or
  loss.
• Non-fluent (minimal speech activity with slow
  speech that requires obvious effort)
• Fluent- (speech is present, but contains little
  meaningful communication).

42
Communication

• Conductive aphasia- mixture of both expressive
  and receptive aphasia
• Global aphasia- results from a massive lesion and
  there is virtual loss of all language ability.

43
Communication, contd

• Wernickes area damage
• Receptive aphasia where neither the sound or
  speech or its meaning can be understood.
• Impaired comprehension of both spoken and written
  language.
• Bocas area damage
• Expressive aphasia (difficulty speaking and
  writing)
• Dysarthria- disturbance in muscular control of
  speech. (pronunciation, articulation, phonation)
  DOES NOT EFFECT COMPREHENSION OF LANGUAGE.

44
(No Transcript)
45
Affect

• May be unable to control emotions
• May be depressed RT body image and loss of
  function
• May be frustrated RT immobility and communication
  issues

46
Intellectual Function

• Memory and judgment may be impaired
• Left-sided stroke patients are more cautious in
  judgment and movement.
• Right-sided stroke patients more impulsive and
  move quicker.

47
Spatial-Perceptual Alterations

• Right sided stroke patient has more
  spatial-perceptual orientation issues
• Erroneous perception of self and illness (may
  deny illness or body parts).
• Erroneous perception of self in space (may ignore
  affected side cant judge distances)
• Agnosia or inability to recognize an object by
  sight, touch or hearing.
• Apraxia or the inability to carry out learned
  sequential movements on command.

48
Elimination

• Most occur initially and are transient.
• Frequent constipation DT immobility, weak
  abdominal muscles, dehydration, and diminished
  defecation reflexes.
• Urinary and bowel elimination may be DT
  functional inabilities to express needs and
  manage clothing.

49
Diagnostic Studies

• CT Scan- indicate size and location of lesion,
  differentiates between infarct and hemorrhage,
  effectiveness of treatment, and evaluate the
  course of healing.
• MRI- considered best method to differentiate
  between hemorrhage and infarct.

50
Diagnostics

• PET shows chemical activity and depicts extent if
  tissue damage.
• DSA- IV or arterial injection of contrast
  material to visualize blood vessels.
• TDA- transcranial doppler measures velocity of
  cerebral blood flow in the arteries, also detects
  micro-emboli.
• LP may be done to detect blood or WBCs (not done
  if increased ICP is suspected)

51
(No Transcript)
52
Collaborative care

• PREVENTION
• Healthy diet
• Weight control
• Regular exercise
• No SMOKING
• Limiting alcohol
• Routine health assessment

53
DRUG THERAPY

• Prophylactic low dose aspirin, daily.
• Persantine 50 mg 3 X day decreases platelet
  aggregation which helps to decrease risk of
  thrombus and embolus formation.
• TICLID or PLAVIX- platelet aggregation inhibitors

54
Surgical Therapy

• Carotid endarterectomy (CEA)- the atheromatous
  lesion is removed from the carotid artery to
  improve blood flow
• Decreases stroke and death in patient with TIAs.
• Done on patient with 70-99 occlusion

55
Transluminal Angioplasty

• Insertion of balloon to open stenosed artery to
  permit blood flow.
• Patient with symptomatic stenosis of
  vertebrobasilar or carotid arteries
• Risk of dislodging emboli

56
EC-IC BYPASS

• Extracranial-intracranial bypass
• Used when obstruction cannot be removed directly
• A branch of extracranial artery is anastomosed to
  a branch of intracranial artery just beyond the
  area of obstruction.
• Patients at high risk for stroke and require
  close-long term assessment and management.

57
ACUTE CARE

• Table 55-5 Lewis page 1654.
• Initially
• Ensure patent airway DT altered level of
  consciousness.
• Remove dentures
• Administer oxygen via nasal cannula or
  non-rebreather mask DT respiratory distress

58
Acute Care

• Establish IV access with normal saline to
  maintain BP
• Remove clothing
• Obtain immediate CT Scan
• Monitor VS, LOC, O2 sats, cardiac rhythms,
  Glasgow Coma Scale, pupil size and reactivity.

59
Acute Care

• Maintain patient warmth
• Reassure patient and family

60
Ischemic Cascade

• Series of events in response to thrombotic and
  embolic strokes.
• Ischemic area becomes discolored and soft,
  initially. However, around the border there is an
  area of perfusion called the ischemic penumbra
  that maintains perfusion for 3 to 6 hours post
  stroke.
• If adequate blood flow is reinitiated during this
  period, less neuro damage results

61
Treatment

• Control fluid and electrolyte balance
• Adequate hydration promotes perfusion to the
  brain however over hydration may increase
  cerebral edema!
• Total intake (oral, tube feedings, IV etc.,
  1500-2000 per day)
• Monitor urine output ( if ADH released urine
  output will decrease)

62
Treatment

• IV solutions with glucose and water are avoided.
  (hypertonic solutions may increase cerebral
  edema)
• Increased ICP from cerebral edema peaks in 72
  hours and may cause brain herniation.

63
How to manage ICP

• Enhance venous drainage by
• Elevating HOB
• Maintain head and neck in alignment
• Avoidance of hip flexion
• Limit cerebral tissue metabolism and vasodilation
  by
• avoiding hyperthermia, avoiding hypervolemia,
  manage constipation

64
Medications

• Diuretics (decrease cerebral edema)
• Mannitol (Osmitrol)
• Lasix, (Furosemide)
• Dexamethasone for patients with vasogenic edema

65
Drug Therapy

• Thrombolytic therapy
• Recombinant tissue plasminogen activator (t-PA)-
  to re-establish blood flow and prevent cell death
  for patients with ischemic strokes.
• Patients who receive t-PA within 3 hours after a
  stroke more likely to have 32 less injury three
  months after stroke.
• T-PA works by lysis thrombus/clot by binding and
  digesting the fibrin and fibrinogen.

66
t-PA

• Clot specific
• Less likely to cause hemorrhage as compared to
  streptokinase or urokinase.
• Single most important factor is timing!!!

67
t-PA

• Patients are screened for coagulation disorders,
  GI bleeding, and hemorrhagic stroke before
  initiation of treatment.
• Major side effect is cerebral hemorrhage.
• Monitor VS during treatment/ control BP
• O anticoagulants or antiplatelet drug for 25
  hours post treatment.

68
Platelet inhibition/anticoagulant therapy

• Heparin, coumadin, aspirin, ticlipidine (Ticlid),
  clopidrogel (Plavix), dipyridamole (Persantine).
• Contraindicated for patients with hemorrhagic
  strokes
• Monitor PT/ PTT
• Monitor patient for bleeding

69
Drug therapy

• Calcium channel blockers are given for patients
  with hemorrhagic strokes.
• Excess intracellular calcium may be harmful to
  brain tissue.
• Nimodipine (Nimotop) decreases effects of
  vasospasm and minimizes tissue damage.
• Aspirin decreases platelet aggregation at site of
  plaque.

70
Drug therapy

• Tylenol treats hyperthermia
• Dilantin may be given for seizures