Traumatic Brain Injury

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Traumatic Brain Injury

• Pathophysiology OTA Course
• For 4th year students

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Objectives
-To describe the common pathophysiological
features of head injury -To define the
mechanisms of hypoxic-ischaemic damage at
neuronal level -To support the importance of
raused intracranial pressure in the determination
of severity in the outcome in head injured
patients -To define the consequences of
traumatic events - case studies
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How do patients present?

• Obvious--motor vehicle accident, car vs
  pedestrian, fall from height, etc
• Less obvious--sports injuries (football), delayed
  deterioration (epidural)
• Hidden--shaken baby syndrome

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Primary Brain Injury

• Primary
• Focal
• Local signs
• Contra-coup
• Diffuse
• Diffuse axonal injury

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Secondary Brain Injury

• Global
• Hypoxia and ischemia of brain
• Decreased cerebral blood flow due to increased
  intracranial pressure
• Local
• impairment of cerebral blood flow or extra
  cellular milieu due to the presence of injured
  brain
• Biochemical Cascade
• Blood Flow changes (Global/regional)

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Cerebral blood flow

• The brain has the ability to control its blood
  supply to match its metabolic requirements
• Chemical or metabolic byproducts of cerebral
  metabolism can alter blood vessel caliber and
  behavior

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Monro-Kellie doctrine

• Volume of intracranial compartment must remain
  constant because of inelastance of skull
• Normal State- ICV is a balance among blood, brain
  CSF.
• With increase ICV? ICP remains normal till
  compensation can occur
• At the point of decompensation The ICP starts to
  increase.
• The brains compensatory reserve is called
  Compliance

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Intracranial Hypertension

• ICP monitoring and control are the cornerstones
  of TBI management
• Normal ICP
• When to treat?

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Cerebral edema - cytotoxic
Caused mainly by activation of cytokines, ROS and
other pro-inflammatory mediators
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Cerebral edema - vasogenic
Caused mainly by activation of NMDA receptors by
glutamate
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Two clinical types of brain injury

• Closed brain injury
• Open brain injury

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Diffuse axonal injury

• Hallmark of severe Traumatic Brain Injury
• Differential movement of adjacent regions of
  brain during acceleration and deceleration.
• DAI is major cause of prolonged coma after TBI,
  probably due to disruption of ascending reticular
  connections to cortex.