Intracerebral hemorrhage




  Thawatchai Leelawittayanont, B. Pharm, MD
•   Introduction
•   Etiology
•   Pathophysiology
•   Clinical presentation
•   Diagnosis and Imaging
•   Treatment
Introduction
Epidemiology
• Asian countries have a higher incidence of
  intracerebral hemorrhage than other regions
  of the world.
• A higher incidence of intracerebral
  hemorrhage has been noted in Chinese,
  Japanese, and other Asian populations,
  possibly due to environmental factors (eg, a
  diet rich in fish oils) and/or genetic factors.
Epidemiology
• Annually, more than 20,000 individuals in the
  United States die of intracerebral
  hemorrhage.
• Intracerebral hemorrhage has a 30-day
  mortality rate of 44%.
• Pontine or other brainstem intracerebral
  hemorrhage has a mortality rate of 75% at 24
  hours.
• Incidence of intracerebral hemorrhage
  increases in individuals older than 55 years
  and doubles with each decade until age 80
Etiology
• Hypertensive ICH
     • Essential
     • Eclampsia
• Non-hypertensive ICH
  – Vascular malformation: AVM, Aneurysm,
    Cavernous hemangioma
  – Bleeding disorders/anticoagulant
  – Amyloid angiopathy
  – Trauma
  – Tumor
  – Drug abuse: amphetamine, cocaine, PPA
Pathophysiology
• Primary immediate effect
  – Hemorrhage growth
  – Increase ICP
• Secondary effect
  – Downstream effect
  – Edema
  – Ischemia
Hemorrhage growth
•   basal ganglia (40-50%),
•   lobar regions (20-50%),
•   thalamus (10-15%),
•   pons (5-12%),
•   cerebellum (5-10%),
•   other brainstem sites (1-5%).
Clinical presentation
• Alteration in level of consciousness
  (approximately 50%)
• Nausea and vomiting (approximately 40-50%)
• Headache (approximately 40%)
• Seizures[3] (approximately 6-7%)
• Focal neurological deficits
Focal neurological deficits
• Putamen - Contralateral hemiparesis,
  contralateral sensory loss, contralateral
  conjugate gaze paresis, homonymous
  hemianopia, aphasia, neglect, or apraxia
• Thalamus - Contralateral sensory loss,
  contralateral hemiparesis, gaze paresis,
  homonymous hemianopia, miosis, aphasia, or
  confusion
Focal neurological deficits
• Lobar - Contralateral hemiparesis or sensory
  loss, contralateral conjugate gaze paresis,
  homonymous hemianopia, abulia, aphasia,
  neglect, or apraxia
• Caudate nucleus - Contralateral hemiparesis,
  contralateral conjugate gaze paresis, or
  confusion
Focal neurological deficits
• Brain stem - Quadriparesis, facial weakness,
  decreased level of consciousness, gaze
  paresis, ocular bobbing, miosis, or autonomic
  instability
• Cerebellum - Ataxia, usually beginning in the
  trunk, ipsilateral facial weakness, ipsilateral
  sensory loss, gaze paresis, skew deviation,
  miosis, or decreased level of consciousness
Investigation
• Laboratory studies
  – CBC
  – Coagulogram
  – Electrolyte
  – others
• Imaging
  – CT brain w/o contrast
CT-brain
• demonstrates acute hemorrhage as
  hyperdense signal intensity
• Multifocal hemorrhages at the frontal,
  temporal, or occipital poles suggest a
  traumatic etiology.
• Hematoma volume can be approximated by (A
  x B x C)/2
• Iodinated contrast may be injected to increase
  screening yield for underlying tumor or
  vascular malformation.
Vessel imaging
• CT angiography permits screening of large and
  medium-sized vessels for AVMs, vasculitis,
  and other arteriopathies.
Intracerebral hemorrhage
Intracerebral hemorrhage
Intracerebral hemorrhage
Intracerebral hemorrhage
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Intracerebral hemorrhage
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Intracerebral hemorrhage
Intracerebral hemorrhage
Intracerebral hemorrhage
Intracerebral hemorrhage

Intracerebral hemorrhage

  • 1.
    Intracerebral hemorrhage Thawatchai Leelawittayanont, B. Pharm, MD
  • 2.
    Introduction • Etiology • Pathophysiology • Clinical presentation • Diagnosis and Imaging • Treatment
  • 3.
  • 4.
    Epidemiology • Asian countrieshave a higher incidence of intracerebral hemorrhage than other regions of the world. • A higher incidence of intracerebral hemorrhage has been noted in Chinese, Japanese, and other Asian populations, possibly due to environmental factors (eg, a diet rich in fish oils) and/or genetic factors.
  • 5.
    Epidemiology • Annually, morethan 20,000 individuals in the United States die of intracerebral hemorrhage. • Intracerebral hemorrhage has a 30-day mortality rate of 44%. • Pontine or other brainstem intracerebral hemorrhage has a mortality rate of 75% at 24 hours. • Incidence of intracerebral hemorrhage increases in individuals older than 55 years and doubles with each decade until age 80
  • 6.
    Etiology • Hypertensive ICH • Essential • Eclampsia • Non-hypertensive ICH – Vascular malformation: AVM, Aneurysm, Cavernous hemangioma – Bleeding disorders/anticoagulant – Amyloid angiopathy – Trauma – Tumor – Drug abuse: amphetamine, cocaine, PPA
  • 7.
    Pathophysiology • Primary immediateeffect – Hemorrhage growth – Increase ICP • Secondary effect – Downstream effect – Edema – Ischemia
  • 8.
  • 9.
    basal ganglia (40-50%), • lobar regions (20-50%), • thalamus (10-15%), • pons (5-12%), • cerebellum (5-10%), • other brainstem sites (1-5%).
  • 10.
    Clinical presentation • Alterationin level of consciousness (approximately 50%) • Nausea and vomiting (approximately 40-50%) • Headache (approximately 40%) • Seizures[3] (approximately 6-7%) • Focal neurological deficits
  • 11.
    Focal neurological deficits •Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia • Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion
  • 12.
    Focal neurological deficits •Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia • Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
  • 13.
    Focal neurological deficits •Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability • Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness
  • 14.
    Investigation • Laboratory studies – CBC – Coagulogram – Electrolyte – others • Imaging – CT brain w/o contrast
  • 15.
    CT-brain • demonstrates acutehemorrhage as hyperdense signal intensity • Multifocal hemorrhages at the frontal, temporal, or occipital poles suggest a traumatic etiology. • Hematoma volume can be approximated by (A x B x C)/2 • Iodinated contrast may be injected to increase screening yield for underlying tumor or vascular malformation.
  • 16.
    Vessel imaging • CTangiography permits screening of large and medium-sized vessels for AVMs, vasculitis, and other arteriopathies.