Traumatic Brain Injury

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Presentation transcript:

Traumatic Brain Injury Pathophysiology OTA Course For 4th year students

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

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

Primary Brain Injury Primary Focal Diffuse Local signs Contra-coup Diffuse axonal injury

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)

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

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

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

Cerebral edema - cytotoxic Caused mainly by activation of cytokines, ROS and other pro-inflammatory mediators

Cerebral edema - vasogenic Caused mainly by activation of NMDA receptors by glutamate

Two clinical types of brain injury Closed brain injury Open brain injury

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.