1. Traumatic Brain Injury
Pathophysiology OTA Course
For 4th year students

2. 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

3. 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

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

5. 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)

6. 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

7. 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

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

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

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

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

12. 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.