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CEREBROVASCULAR ACCIDENT
    OR ―BRAIN ATTACK‖
  Third leading cause of death

 750, 000 cases/year
 Leading cause of significant disability
 Cost: $40 billion/year
Types of Stroke
  Ischemic, 80%

   - thrombosis, 50% (small & large-vessel)
   - embolism, 30%
 Hemorrhagic, 20%
   - intracerebral (HTN as risk)
   - subarachnoid (aneurysm)
CEREBRAL HEMORRHAGE
  HEMORRHAGIC STROKE

 PRIMARY INTRACEREBRAL
  HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
  AMYLOID ANGIOPATHY
CEREBRAL HEMORRHAGE
  HEMORRHAGIC STROKE

 PRIMARY INTRACEREBRAL
  HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
  AMYLOID ANGIOPATHY
HEMORRHAGIC STROKE
  The transformation of a bland infarct into a

  hemorrhagic infarct is a common
  occurrence (highest in autopsy studies)
 ―The concept of migratory embolus‖
Right Middle Cerebral Artery Territory Infarct
Risk Factors For Hemorrhagic
    Transformation of a Bland Infarct
  Advanced age

 Embolization as etiology
 High systolic BP
 CT shows mass effect
 Larger territory strokes
 Anticoagulation
 History of coagulopathy
HEMORRHAGIC INFARCT
CEREBRAL HEMORRHAGE
  HEMORRHAGIC STROKE

 PRIMARY INTRACEREBRAL
  HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
  AMYLOID ANGIOPATHY
RISK FACTORS FOR ICH
  Advancing age

 HTN (autopsy studies on patients with ICH
  showed high incidence of LVH;
  PROGRESS – Perindopril Protection
  Against Recurrent Stroke Study:76%
  relative risk reduction of ICH in
  comparison to placebo
 Cigarette smoking
 alcoholism
PRIMARY INTRACEREBRAL
          HEMORRHAGE
    Five most common sites:

    putamen: 35 % - 50%
    subcortical white matter 30%
    thalamus: 10%-15%
    pons 5%-12%
    cerebellar white matter <5%
THE ANTERIOR CIRCULATION
Most ICH originate from the rupture of

  small deep penetrating arteries (50 to 200
  um); most common: lenticulostriates
 Same arteries are recognized to be
  occluded in lacunar infarcts (process:
  fibrinoid necrosis or lipohyalinosis)
Massive Right Putaminal Hemorrhage
Subcortical White Matter ICH
Pontine Hemorrhage
Thalamic Hemorrhage
Right Cerebellar Hemorrhage
CEREBRAL HEMORRHAGE
  HEMORRHAGIC STROKE

 PRIMARY INTRACEREBRAL
  HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
  AMYLOID ANGIOPATHY
SUBARACHNOID HEMORRHAGE
  Accounts for 5-10% of all strokes

 Incidence has not declined in 30 years
 80% due to rupture of intracranial saccular
  aneurysm
 30-day mortality rate 50%
 Most deaths occur within one week
RUPTURED ANEURYSM SITES: International
    Cooperative Study On The Timing Of Aneurysm Study

  Anterior communicating artery (ACom)

  34%
 ICA 30%
 MCA 22%
 Basilar tip, PICA, basilar trunk branches—
  7.6%
CAUSES OF SUDDEN DEATH IN SAH

  Large intraparenchymal hematoma

 Destruction of brain tissue
 Acute hydrocephalus
 Increased intracranial pressure
 Cardiac arrhythmias, MI, PE and
  respiratory failure
LEADING CAUSES OF DEATH ON
       HOSPITALIZED PATIENTS
  Sequelae of initial hemorrhage

 Recurrent aneurysmal
 Vasospasm leading to ischemic stroke
 Severe medical complications
CEREBRAL HEMORRHAGE
  HEMORRHAGIC STROKE

 PRIMARY INTRACEREBRAL
  HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
  AMYLOID ANGIOPATHY
CEREBRAL AMYLOID ANGIOPATHY

  Amyloid deposition in the cerebral vessels

  sufficient to cause symptomatic vascular
  dysfunction
 Vessel rupture and spontaneous ICH
  untreatable and unpreventable
 Prevalence of CAA: 2.3% age 65-74; 8%
  age 75-84 ;12.1% 85 and older
HEMORRHAGE SECONDARY TO CEREBRAL
         AMYLOID ANGIOPATHY (CAA)

  Most common cause of lobar

  hemorrhages in non-hypertensive
  individuals
 Elderly patients
 Evidence of small microbleeds in MRI
 Long-term recurrence increased
RISK FACTORS FOR CAA LOBAR
            HEMORRHAGE
  Advanced age

 APOE epsilon2 or epsilon4
 Alzheimer’s disease
RISK FACTORS FOR NON-CAA ICH

  Family history of ICH

 Frequent use of alcohol
 Previous ischemic stroke
 Low serum cholesterol level
ICH: EVALUATION AND WORK-UP:

    History and PE

    Computed Tomography (CT) scan of the head

    12-lead EKG, chest X-ray

    Complete blood count, PT, PTT

    Chemistries (sodium, phosphate, glucose

    abnormalities may mimic stroke)
    Urine and serum toxicology (drugs and alcohol)

Other Neuroimaging Techniques &
         Ancillary Tests
  Magnetic Resonance Imaging (MRI)

  Diffusion Weighted Imaging (DWI),
  Magnetic Resonance Angiography (MRA)
 Ultrasound (Carotid Duplex, Transcranial
  Doppler, 2-D echo)
 Conventional Angiography
SUBACUTE INTRACEREBRAL HEMORRHAGE
Under special circumstances, the
    following tests may be required:
  Cervical spine x-ray

 Arterial blood gas
 Lumbar puncture
 Electroencephalogram (EEG)
Glasgow Coma Scale

               1               2                 3                  4                 5                 6




                               Opens eyes in     Opens eyes in
               Does not open                                        Opens eyes
Eyes                           response to       response to                          N/A               N/A
               eyes                                                 spontaneously
                               painful stimuli   voice




                                               Utters                                 Oriented,
               Makes no        Incomprehensibl                      Confused,
Verbal                                         inappropriate                          converses         N/A
               sounds          e sounds                             disoriented
                                               words                                  normally




                                                 Abnormal           Flexion /
               Makes no        Extension to                                           Localizes         Obeys
Motor                                            flexion to painful Withdrawal to
               movements       painful stimuli                                        painful stimuli   Commands
                                                 stimuli            painful stimuli
Overview of ICH Management
    ICH has frequent early, ongoing bleeding and
    progressive deterioration, severe clinical deficits
    and subsequent high mortality and morbidity
    rates
    Good general supportive management (airways,

    oxygenation, circulation, glucose level, fever, DVT
    prophylaxis)
    Slowing or stopping initial bleeding

    Blood removal from parenchyma or ventricles

    Management of complications of blood in the rain

    (increased ICP, decreased CPP)
CASE SPECIFIC MANAGEMENT

  Correctible/controllable causes of

  hemorrhage (e.g. warfarin)
 Clipping of aneurysm
Herniation
  Early clinical signs: mental status change,

  pupillary dilatation, vomiting
 Late clinical signs: ocular paresis,
  decerebrate rigidity, coma and death
TREATMENT OF BRAIN
              SWELLING
     Cerebral perfusion pressure =MAP-ICP
    Fluid Restriction (1200 ml /day/m2)

    Controlled hyperventilation: 25 mm Hg

    Mannitol, 0.25 mg/kg IV over 20 minutes; repeat PRN,

    serum osmolality maintained in the range of 300-
    320mOsm/l
    Barbiturate coma, with ICP monitoring (subrachnoid bolt,

    IV catheter or Camino catheter): maintain CPP greate
    than 50 mmHg; pentobarbtial serum level of 2-4 mg/dl
    Drainage of CSF (ventriculostomy)

    Lobectomy

Before Intraven-
tricular TPA




After
INTRAVENTRICULAR HEMORRHAGE

Intracerebral hemorrhage has
     frequent early, ongoing
    bleeding and progressive
  deterioration, severe clinical
 deficits and subsequent high
 mortality and morbidity rates.
THANK YOU!

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Cerebral Hemorrhage By Arlyn M. Valencia, M.D. Associate Professor, University Of Nevada School Of Medicine

  • 1.
  • 2. CEREBROVASCULAR ACCIDENT OR ―BRAIN ATTACK‖ Third leading cause of death   750, 000 cases/year  Leading cause of significant disability  Cost: $40 billion/year
  • 3. Types of Stroke Ischemic, 80%  - thrombosis, 50% (small & large-vessel) - embolism, 30%  Hemorrhagic, 20% - intracerebral (HTN as risk) - subarachnoid (aneurysm)
  • 4. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  • 5. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  • 6. HEMORRHAGIC STROKE The transformation of a bland infarct into a  hemorrhagic infarct is a common occurrence (highest in autopsy studies)  ―The concept of migratory embolus‖
  • 7. Right Middle Cerebral Artery Territory Infarct
  • 8.
  • 9. Risk Factors For Hemorrhagic Transformation of a Bland Infarct Advanced age   Embolization as etiology  High systolic BP  CT shows mass effect  Larger territory strokes  Anticoagulation  History of coagulopathy
  • 11.
  • 12.
  • 13. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  • 14. RISK FACTORS FOR ICH Advancing age   HTN (autopsy studies on patients with ICH showed high incidence of LVH; PROGRESS – Perindopril Protection Against Recurrent Stroke Study:76% relative risk reduction of ICH in comparison to placebo  Cigarette smoking  alcoholism
  • 15. PRIMARY INTRACEREBRAL HEMORRHAGE Five most common sites:  putamen: 35 % - 50% subcortical white matter 30% thalamus: 10%-15% pons 5%-12% cerebellar white matter <5%
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  • 17.
  • 19. Most ICH originate from the rupture of  small deep penetrating arteries (50 to 200 um); most common: lenticulostriates  Same arteries are recognized to be occluded in lacunar infarcts (process: fibrinoid necrosis or lipohyalinosis)
  • 20.
  • 25.
  • 27. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  • 28. SUBARACHNOID HEMORRHAGE Accounts for 5-10% of all strokes   Incidence has not declined in 30 years  80% due to rupture of intracranial saccular aneurysm  30-day mortality rate 50%  Most deaths occur within one week
  • 29. RUPTURED ANEURYSM SITES: International Cooperative Study On The Timing Of Aneurysm Study Anterior communicating artery (ACom)  34%  ICA 30%  MCA 22%  Basilar tip, PICA, basilar trunk branches— 7.6%
  • 30.
  • 31.
  • 32. CAUSES OF SUDDEN DEATH IN SAH Large intraparenchymal hematoma   Destruction of brain tissue  Acute hydrocephalus  Increased intracranial pressure  Cardiac arrhythmias, MI, PE and respiratory failure
  • 33. LEADING CAUSES OF DEATH ON HOSPITALIZED PATIENTS Sequelae of initial hemorrhage   Recurrent aneurysmal  Vasospasm leading to ischemic stroke  Severe medical complications
  • 34.
  • 35. CEREBRAL HEMORRHAGE HEMORRHAGIC STROKE   PRIMARY INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  HEMORRHAGE FROM CEREBRAL AMYLOID ANGIOPATHY
  • 36. CEREBRAL AMYLOID ANGIOPATHY Amyloid deposition in the cerebral vessels  sufficient to cause symptomatic vascular dysfunction  Vessel rupture and spontaneous ICH untreatable and unpreventable  Prevalence of CAA: 2.3% age 65-74; 8% age 75-84 ;12.1% 85 and older
  • 37. HEMORRHAGE SECONDARY TO CEREBRAL AMYLOID ANGIOPATHY (CAA) Most common cause of lobar  hemorrhages in non-hypertensive individuals  Elderly patients  Evidence of small microbleeds in MRI  Long-term recurrence increased
  • 38. RISK FACTORS FOR CAA LOBAR HEMORRHAGE Advanced age   APOE epsilon2 or epsilon4  Alzheimer’s disease
  • 39. RISK FACTORS FOR NON-CAA ICH Family history of ICH   Frequent use of alcohol  Previous ischemic stroke  Low serum cholesterol level
  • 40. ICH: EVALUATION AND WORK-UP: History and PE  Computed Tomography (CT) scan of the head  12-lead EKG, chest X-ray  Complete blood count, PT, PTT  Chemistries (sodium, phosphate, glucose  abnormalities may mimic stroke) Urine and serum toxicology (drugs and alcohol) 
  • 41. Other Neuroimaging Techniques & Ancillary Tests Magnetic Resonance Imaging (MRI)  Diffusion Weighted Imaging (DWI), Magnetic Resonance Angiography (MRA)  Ultrasound (Carotid Duplex, Transcranial Doppler, 2-D echo)  Conventional Angiography
  • 42.
  • 44. Under special circumstances, the following tests may be required: Cervical spine x-ray   Arterial blood gas  Lumbar puncture  Electroencephalogram (EEG)
  • 45. Glasgow Coma Scale 1 2 3 4 5 6 Opens eyes in Opens eyes in Does not open Opens eyes Eyes response to response to N/A N/A eyes spontaneously painful stimuli voice Utters Oriented, Makes no Incomprehensibl Confused, Verbal inappropriate converses N/A sounds e sounds disoriented words normally Abnormal Flexion / Makes no Extension to Localizes Obeys Motor flexion to painful Withdrawal to movements painful stimuli painful stimuli Commands stimuli painful stimuli
  • 46. Overview of ICH Management ICH has frequent early, ongoing bleeding and progressive deterioration, severe clinical deficits and subsequent high mortality and morbidity rates Good general supportive management (airways,  oxygenation, circulation, glucose level, fever, DVT prophylaxis) Slowing or stopping initial bleeding  Blood removal from parenchyma or ventricles  Management of complications of blood in the rain  (increased ICP, decreased CPP)
  • 47. CASE SPECIFIC MANAGEMENT Correctible/controllable causes of  hemorrhage (e.g. warfarin)  Clipping of aneurysm
  • 48. Herniation Early clinical signs: mental status change,  pupillary dilatation, vomiting  Late clinical signs: ocular paresis, decerebrate rigidity, coma and death
  • 49. TREATMENT OF BRAIN SWELLING Cerebral perfusion pressure =MAP-ICP Fluid Restriction (1200 ml /day/m2)  Controlled hyperventilation: 25 mm Hg  Mannitol, 0.25 mg/kg IV over 20 minutes; repeat PRN,  serum osmolality maintained in the range of 300- 320mOsm/l Barbiturate coma, with ICP monitoring (subrachnoid bolt,  IV catheter or Camino catheter): maintain CPP greate than 50 mmHg; pentobarbtial serum level of 2-4 mg/dl Drainage of CSF (ventriculostomy)  Lobectomy 
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  • 58. Intracerebral hemorrhage has frequent early, ongoing bleeding and progressive deterioration, severe clinical deficits and subsequent high mortality and morbidity rates.