Download Traumatic Brain Injury

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
• Local signs
• Contra-coup
– Diffuse
• 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.